Biology A2

Chapter 14 – Homeostasis

Organisms need to keep some of their internal conditions near constant.

This allows them to function efficiently.

Control systems are used to maintain these internal conditions, and they contribute to the
overall process of keeping these conditions near constant, homeostasis.

Homeostasis is the maintenance of a relatively constant environment for cells within

the body.

Sensory cells can detect changes in these internal conditions.

They can also acknowledge external surroundings.

Note we have said internal conditions, these are essentially physiological factors within
the body.

These consist of,

 - Core Body Temperature

- Metabolic Wastes (Mainly CO2 and Urea)

- Blood pH

- Blood Glucose Concentration

- Water Potential of Blood

- Concentration of Respiratory Gasses, Oxygen and Carbon Dioxide, within the blood

When we refer to the internal environment within an organism, we are essentially talking
about the internal conditions within the body of the organism.

A cell functions within these conditions.

For a cell, its local environment or its immediate environment is the tissue fluid which
surrounds it.

Features of the tissue fluid influence how efficient or how well the cell functions.

Such features include,

- Temperature

Tissue fluid at a low temperature would slow down metabolic reactions that occur within a
cell.

At a high temperature, proteins within the cell such as enzymes would denature, causing
them to not function.

- Water Potential

At the decrease of water potential of tissue fluid, water will move out of the cells by
osmosis into the tissue fluid.

This will cause METABOLIC REACTIONS IN THE CELL TO SLOW DOWN OR STOP.

If the water potential of tissue fluid increases, water will move into the cells from the
tissue fluid by osmosis.
This will cause the cell to swell and burst.

- Blood Glucose Concentration

Glucose serves as the main respiratory substrate for cells, the main fuel for respiration.

The lack of glucose present within tissue fluid causes respiration to slow down, or even
stop.

This deprives the cell of its energy source.

Too much glucose present within tissue fluid will decrease the water potential of tissue
fluid.

This follows the same effect explained above, water moves out of the cells, causing the
metabolism within them to slow down or even stop.

See the diagram below.

Take note we say blood glucose concentration, because the concentration of glucose within
tissue fluid essentially is reflective of that of the concentration of glucose within the
plasma in the blood.

- The pH of tissue fluid

The activity of enzymes as we know, is affected by pH.

Cytoplasmic pH within cells ranges from 6.5 – 7.0.

If it is to shift away from this range, enzymes will function less efficiently.

At extreme fluctuations from this pH range, the enzymes could denature.

As we have seen a lot of the above factors to be related with blood,

Thus, homeostasis in general essentially acts to control the composition of the blood.

And in turn, the composition of the blood decides (can say control) the composition of
tissue fluid.

Aspects of the blood and hence tissue fluid are controlled by different control systems.

Such aspects consist of the four physiological factors for tissue fluid we have discussed
above.

The majority of control mechanisms make use of a negative feedback loop.

The series of steps that occur within this loop act to maintain hemostatic balance.

Negative feedback is a process in which a factor that brings about change brings
about processes which return said factor back to normal. (its set point).

It essentially is countering the change that caused displacement from the set point.

The loop involves a receptor, which can be thought of as a sensor.

It also involves an effector; these include muscles and glands.

A receptor detects a specific change in its respective environment.

This change is a stimulus.

A receptor that detects a specific stimulus involved with the physiological factor that is
to be maintained or regulated.

The stimulus can be the change in the factors we have considered, such could be the
change in the blood temperature or the water content of the blood.

Receptors can be of two types, external receptors and internal receptors.

They have their respective roles in detecting external stimuli from the surroundings of
the organism or internal stimuli within the organism.

The information receptors sense about changes in their environment is sent off through
the nervous system.

This is to the central controls, located either in the brain or spinal cord.

The sensory information they pass on is defined as the input.

Information can also be sent from receptors through the endocrine system.

A receptor is a cell or tissue that is sensitive to a specific stimulus, (once it senses

this stimulus), it communicates with a control center by the generation of nerve
impulses or the sending of a chemical messenger.

An effector is a tissue or organ that carries out an action in response to a stimulus;

muscles and glands are effectors.

A stimulus is a change in the external or internal environment that is detected by a

receptor, and which may cause a response.

The central control serves to instruct the effector.

The effector carries out an action, or a response.

This is defined as the output.

These actions are also defined as corrective actions.

Their effect is simply to correct or REVERSE the changes that have been detected.

A corrective action is a response or series of responses that return a physiological

factor to the set point so maintaining a constant environment for the cells within the
body.

The set point is the ideal value of a physiological factor that the body controls in
homeostasis.

For a single physiological factor, there is a steady stream of information being sent to the
central control.

This is as there is continuous monitoring from the receptor.

Continuous corrective actions are thus made by the effector, this follows continuous
adjustments to the output.

Due to the above, the factor fluctuates or goes up or down around a particular “ideal”
value.

This ideal value is the set point.

Negative feedback is used by homeostatic mechanisms because it minimizes the
difference between the actual value of the factor and its ideal value or set point.

Negative feedback is essentially maintaining these physiological factors at or near the set
point.

In such a mechanism, an increase in the factor from the set point results in a decrease of
that factor.

A decrease in the factor from the set point results in the increase of that factor.

The factor never stays constant, nor does it stay at its set point.

It fluctuates continuously above and below the set point by a little bit.

Measured in the mouth, the human body temperature (physiological factor) fluctuates
between 36.4 degrees celsius and 37.6 degrees celsius.

This is the often range that is seen, the actual range is dependent on a series of other
factors.

These involves age, sex, and time of day.

Different parts of the body are involved in the transfer of information in hemostatic
mechanisms in mammals.

The two systems within the body that support the transfer of this information involve the,

- Nervous System
 - Endocrine System

Both systems are coordination systems.

The nervous system transmits information in the form of electrical impulses along neurons.

The endocrine system makes use of long-distance cell-signaling, using chemical messengers
called hormones, these travel in the blood.

A hormone is a substance secreted by an endocrine gland that is carried in blood

plasma to another part of the body where it has an effect.

Sometimes negative feedback is not the mechanism that is used by control systems.

We could observe an example of this as to when a person breathes air that has a high
carbon dioxide content.

The person will have a higher CO2 concentration within their blood.
The change in such physiological factor is picked up by carbon dioxide receptors.

This leads to the eventual response of increasing the breathing rate.

The person breathes faster, taking in more carbon dioxide, this further stimulates the
receptors.

The person breathes faster....and faster.

Such is the example of positive feedback.

It can’t play a role as shown by this example, in keeping conditions within the body
constant.

Positive feedback is a process in which a change in some parameter such as a

physiological factor brings about processes that move its level further in the direction
of the initial change.

Most metabolic reactions that occur within our body produce unwanted substances.

These are wastes.

Some of them are toxic or poisonous.

The removal of such waste is termed as excretion.

Excretion is the removal of toxic or waste products of metabolism from the body.

Though many excretory products are made in humans, the ones formed in most quantity
are CO2 and urea.

CO2 is a waste product of the respiration of aerobic cells.

It is transported from these respiring cells to the lungs via the bloodstream.

The exchange of gas within the lungs causes CO2 to diffuse into the alveoli from the blood.

It is then excreted with the air we breathe out.

An excess of amino acids produces urea.

It is produced within the liver.

Within the blood plasma, it is transported from the liver to the kidneys.

The kidneys filter the urea from the blood and excrete it in dissolved water.

The overall solution that is excreted is urine.

Excess protein can’t be stored within the body.

Though since amino acids can serve as respiratory substrates to provide useful energy, it
would be wasteful to get rid of all this excess.

To make use of the energy that is within these amino acids, the liver removes the amine
groups present in these amino acids.
This is by a process known as deamination.

The image above serves as a display of how deamination takes place.

The amine group (-NH2) of the amino acid is removed, along with a hydrogen atom.

Together these combine to produce ammonia.

The keto acid that is produced as a result of this can be respired directly, converted into
glucose, converted to glycogen, or converted to fat for storage.

Ammonia though, is a problem.

It is a very soluble and toxic compound.

In many aquatic animals, ammonia diffuses from the blood and dissolves in the water that
surrounds the animal.
Though in land or terrestrial animals, such as us, ammonia increases the pH within the
cytoplasm of cells.

It interferes with metabolic processes; it also disrupts cell signaling in the brain.

Such damage is prevented by the immediate conversion of ammonia into urea IN THE
LIVER.

Urea is less soluble, and less toxic.

This involves a series of reactions which are involved in the urea cycle, though the overall
process is the combination of ammonia with carbon dioxide.

This produces urea.

An adult human produces 20-25 g of ammonia per day.

Urea is the main nitrogenous excretory product of humans.

Other excretory nitrogenous substances are produced, such could be creatinine and uric
acid.

CREATINE, we are finally upon your knowledge.

Creatine is a substance that is made in the liver.

It is made from certain amino acids.

Much creatine serves its role as creatine phosphate in the muscles, this acts as an energy
store.

Though, some of this creatine is converted into creatinine and excreted.

Uric acid is made from the breakdown of not amino acids, but purine bases from
nucleotides.

Urea is a nitrogenous excretory product produced in the liver from the deamination of
amino acids,

Deamination is the breakdown of excess amino acids in the liver, by the removal of
the amine group; ammonia and, eventually, urea are formed from the amine group.

Urea produced by deamination diffuses from the liver cells into the blood plasma.

Despite being less soluble and less toxic than ammonia, it is still soluble and toxic.

The concentration of urea could build up and become dangerous.

This is if not all of it is excreted each day it is produced.

As blood passes through the kidneys, the urea gets filtered.

This produces urine, which is excreted.

The above image shows us the position of the kidneys within the body.

It also displays and annotates structures that are related to the kidneys.

Kidneys receive blood from the renal artery (red), and blood is returned from them by the
renal vein (blue).

Going out of the kidneys is a narrow tube, this is the ureter.

It carries urine from the kidneys to the bladder.

From the bladder, urine is carried in a single tube, this is the urethra.
As we observe the longitudinal section of a kidney, we see that the kidney has 3 main
areas.

Beneath a quite tough fibrous capsule, lies the cortex of the kidney.

The central space or area within the kidney is made up of the medulla.

The ureter joins at an area termed as the renal pelvis.

When observing a section through a kidney (into the kidney) with a microscope, thousands
of blood vessels and tubules are observed.

These tubules are nephrons.

The image above displays the position of a SINGLE nephron within the kidney.

The image that follows it outlines its structure.

At one end of the nephron tubule, the end forms a cup-shaped structure.

This is defined as Bowman’s capsule.

This shaped structure surrounds a network of capillaries.

This network is defined as the glomerulus.

All the glomeruli and capsules OF all the nephrons within the kidney, reside in the cortex
of the kidney.

Take note the glomeruli and capsules serve only part of the nephron’s structure; they
reside in the cortex though the entire nephron does not solely reside in the cortex.

The tubule continues from the capsule towards the center of the kidney.

As it does this, it firstly forms a twisted region.

This is defined as the proximal convoluted tubule.

It then forms a long U-shaped tubule, which is within the medulla.

This is the loop of Henle.

The first part of such loop is defined as the descending limb, it runs down into the
medulla.

The second part is the ascending limb, which runs back into the cortex.

As the ascending limb rises back up, another twisted region is formed.

This is the distal convoluted tubule.

This region joins with the collecting duct, which now leans down into the medulla directly
into the renal pelvis.

A nephron is the structural and functional unit of the kidney composed of Bowman’s
capsule and a tubule divided into three regions: proximal convoluted tubule, loop of
Henle and distal convoluted tubule.

Bowman’s capsule is the cup-shaped part of a nephron that surrounds a glomerulus

and collects filtrate from the blood.

The glomerulus is a group of capillaries within the ‘cup’ of a Bowman’s capsule in the
cortex of the kidney.

The proximal convoluted tube is the part of the nephron that leads from Bowman’s
capsule to the loop of Henle.

The loop of Henle is the part of the nephron between the proximal and distal
convoluted tubules.

The distal convoluted tube is the part of the nephron that leads from the loop of
Henle to the collecting ducts.

The collecting duct is the tube in the medulla of the kidney that carries urine from
the distal convoluted tubules of many nephrons to the renal pelvis.
The first image above shows the cross section of the cortex of the kidney.

It shows a glomerulus and Bowman’s capsule surrounded by proximal and distal convoluted
tubules.

The distal convoluted tubules appear with a lighter lumen while the proximal convoluted
tubules have more of a fuzzy lumen.

Within the glomerulus are red blood cells WITHIN CAPILLARIES.

The outer surface of the capillaries is lined with podocyte cells, these serve as
components for the bowman’s capsule.

The second image shows us the cross section through the medulla of the kidney.

Here we observe the collecting duct and the loop of Henle.

There are also capillaries which are visible.

As we can observe from the image above, blood vessels are quite closely associated with
nephrons.

Within the nephrons in the kidney, each glomerulus at the cortex is supplied from a branch
of the renal artery.

This is THROUGH an afferent arteriole.

The capillaries of the glomerulus proceed to rejoin to form the efferent arteriole.

Blood then flows from this arteriole into a network of capillaries.

This network runs closely alongside the rest of the nephron along with the collecting duct.
Blood from these capillaries then eventually flows through venules in the kidney, and blood
eventually leaves the kidney through a branch of the renal vein.

The afferent arteriole is the arteriole leading to the glomerular capillaries.

The efferent arteriole is the arteriole leading away from glomerular capillaries.

Urine is made in the kidneys by a 2 stage process.

The first stage is ultrafiltration, it involves filtering small molecules.

Ultrafiltration is filtration on a molecular scale separating small molecules from larger

molecules, such as proteins (e.g. the filtration that occurs as blood flows through
capillaries, especially those in glomeruli in the kidney).

From these small molecules is urea, it is filtrated out of the blood and into the Bowman’s
capsule.

Ultrafiltration leads to the formation of filtrate.

The filtrate then flows from the bowman capsule along the nephron toward the collecting
duct.

The second stage of making urine is termed selective reabsorption.

This involves taking back any useful molecules from the filtrate as it flows along the
nephron.

The above images will serve as a reference to us as we explain ultrafiltration.

In the performance of ultrafiltration, small molecules are filtered to form a filtrate in the
bowman’s capsule.
The blood that withholds these small molecules is separated from the lumen of the
bowman’s capsule by two cell layers and a basement membrane. (two cell layers close a
sandwich of basement membrane).

Firstly, we have the cell layer which lines the inner surface of capillaries.

This is the endothelium of the capillary; it is made up of endothelial cells.

Each endothelial cell is pierced or perforated.

This is by many tiny holes which line up with the basement membrane.

These holes are circular, and they are about 60-80 nm in diameter.

Now we approach our meat between buns, the basement membrane.

It is made up of a network of collagen and glycoproteins.

The second layer of cells is made up of epithelial cells.

These make up the inner lining of the bowman’s capsule.

Though, “epithelial cell” is more of a general name for these cells.

This is as these cells have tiny finger like projections.

Gaps are present between these cells.

These cells are termed podocyte cells.

In the image below you can observe podocyte cells (blue-green) at the outside surface of
blood capillaries (purple), the extensions or finger like projections are wrapped around the
capillary.
A podocyte is one of the cells that makes up the lining of Bowman’s capsule
surrounding the glomerular capillaries.

The holes that are present within the endothelium lining of the capillary, along with the
gaps present between podocyte cells make it relatively easy for substances that are
dissolved in the blood plasma.

These substances can now pass from the blood in the glomerular capillaries into the lumen
of the bowman’s capsule.

THOUGH HOWEVER, large protein molecules are not allowed to pass through.

This is as these protein molecules are prevented from passing by the basement membrane
present between the two cell layers.

Protein molecules that have a relative molecular mass of greater than 69 000, can’t pass
through the basement membrane and thus they can’t leave the glomerular capillaries.

So, as we have defined ultrafiltration as the filtration of small molecules to form a

filtrate within the bowman’s capsule, our basement membrane ACTS AS OUR FILTER.

Red and White blood cells are halted by the endothelium lining of the capillary.

This is as they are too fat to pass through the perforations present within the endothelial
cells or the endothelium. (as a whole).

Thus, they remain within the blood.

The table above displays the concentrations of substances within the blood present in the
glomerular capillaries and that of those substances present in the glomerular filtrate
within the bowman capsule’s lumen.

It can be simply observed that the composition of the glomerular filtrate is identical to
that of the blood plasma.

The only difference be that there are almost no plasma proteins present within the
glomerular filtrate.

We defined the glomerular filtration rate as the rate at which fluid present within the
blood plasma within the glomerular capillaries filters into the lumen of the bowman’s
capsule.

This rate is essentially dependent on the difference in water potential between the
glomerular capillaries and the filtrate of the bowman’s capsule.

We must consider that,

Water moves from a region of high potential to a region of low potential.

Water potential is decreased by the presence of solutes, and it is increased due to

increases in pressure.
The blood pressure within the glomerular capillaries is relatively high.

This is as blood flows from the afferent arteriole through the glomerular capillaries into
the efferent arteriole.

The afferent arteriole is wider than the efferent arteriole.

This causes pressure to increase within the glomerular capillaries such that, the water
potential of the blood plasma within the capillaries becomes GREATER than the water
potential of the filtrate present in the bowman’s capsule.

SEE BELOW

Though, we must also now consider that the concentration of solute present within the
blood plasma of the glomerular capillaries is greater than that of the concentration of
solute present within the bowman’s capsule.

This is as despite most of the content of the blood plasma can filter through the
basement membrane, going into the capsule, plasma proteins from the blood plasma can’t
filter through.

This is as they are too big, and they thus stay in the blood.
Such a difference in solute concentration tends to make the water potential present
within the glomerular capillaries LOWER than that of the water potential of the filtrate
within the bowman’s capsule.

Though overall, the water potential of within the glomerular capillaries is higher than
that of the water potential present in the filtrate of the bowman’s capsule.

This is as the effect of pressure CANCELS OUT the effect of solute concentration.

AS A RESULT, WATER MOVES DOWN ITS POTENTIAL GRADIENT FROM THE

GROMELULAR CAPILLARIES INTO THE LUMEN OF THE BOWMAN’S CAPSULE AS
BLOOD FLOWS THROUGH THE GLOMERULUS.

Many of the substances present within the glomerular filtrate are still needed by the
body.

They are thus reabsorbed back into the blood as the filtrate passes along the nephron.

Despite being the majority, only certain substances are needed to be kept, and only they
are reabsorbed.

This is why such a process is termed selective reabsorption.

Most reabsorption takes place in the proximal convoluted tubule.

The lining that makes up the PCT is made up of a single layer of cuboidal epithelial cells.

The cells have adaptivity when it comes to reabsorption.

This is as they have,

- Numerous microvilli on their surfaces that surround the lumen of the nephron.

These microvilli serve as extensions from the membranes of these epithelial cells.

These membranes of these epithelial cells are defined as luminal membranes.

These are membranes which are oriented (faced) towards the lumen.

- Many co-transporter proteins.

- Tight junctions in between cells.

These tight junctions hold adjacent cells firmly together.

This is so that every substance that is to be absorbed must go through or into the cells.

Fluid can’t pass in between the cells.

- Many mitochondria.
These are used to provide energy for sodium-potassium protein pumps.

Such pumps are present within the basal (at base) membranes of the epithelial cells.

Blood capillaries lie close to the proximal convoluted tubule.

Within these capillaries is blood that comes directly from the capillaries present within
the glomerulus.

Due to the ultrafiltration of the blood plasma of the glomerulus, the blood within these
capillaries has much less plasma (general), water, solutes, and ions.

Remember, that if fluid from the blood entered the glomerular filtrate through a solute concentration gradient, this would not cause an
EXCESS in the loss of water, ions, and solutes.

The water potential and solute concentration would hence be balanced between the blood plasma and the filtrate.

This would not permit the reabsorption of glucose by diffusion down its concentration gradient from the cuboidal epithelial cell and into the
blood capillary.

The basal membranes of the cuboidal epithelial cells are the closest to the blood
capillaries alongside the tubule.

Sodium-potassium pumps present on these membranes pump Na+ and K+ ions.

The pumping of Na+ ions cause them to go out of the cells.

They are carried away by the blood in the capillaries present outside.

Such pumping causes the decrease of the sodium ion concentration present within the
epithelial cells.

These cells as a recall, make up the lining of the PCT.

The decrease in concentration of sodium ions within the cells causes the diffusion of
sodium ions.

FROM THE FILTRATE IN THE LUMEN

THROUGH THE LUMINAL MEMBRANE OF THE EPITHELIAL CELLS

INTO THE EPITHELIAL CELLS.

Though, the sodium ions can’t diffuse freely through the membrane into the cells.

They only enter with the support of co-transporter proteins.

These are present within the luminal membranes of the epithelial cells.

Sodium diffuses down its concentration gradient along with another substance through the
co-transporter protein.

This other substance could be glucose, or a specific type of amino acid.

The substance is necessary for the diffusion of sodium to occur through the

co-transporter protein.

The passive movement of the sodium ions down their concentration gradient provides
energy for the movement of the substance it travels with.

This could be glucose or amino acid.

These substances in this way move into the epithelial cell.

The mechanism as such above is an example of indirect or secondary active transport.

This is as the energy provided by ATP is used to pump sodium ions out of the epithelial
cell.

The energy is not used directly to cause the active transport of glucose or amino acid.

Inside the epithelial cell, glucose or amino acid diffuses down its concentration gradient
via a transport protein present in the basal membrane of the cell.

The substance diffuses from the epithelial cell into the blood present within the capillary.
No glucose is present in urine.

This is as all the glucose that was present in the glomerular filtrate was reabsorbed back
into the blood by the above mechanism.

In a similar fashion, amino acids, sodium and chloride ions, and vitamins are reabsorbed
back into the blood from the proximal convoluted tubule.

With the removal of all the solutes above, the water potential of the filtrate passing
through the nephron increases.
The movement of solutes into the blood in the capillary causes the water potential of the
blood to decrease.

A steep water potential gradient is thus established between the filtrate in the nephron
and the blood in the capillary.

Water thus moves FROM THE FILTRATE, THROUGH THE EPITHELIAL CELLS, INTO
THE BLOOD by OSMOSIS.
The water along with the reabsorbed solutes are carried away, back into circulation.

In an odd turn around, quite a lot of urea is reabsorbed.

This is as the cell surface membranes of epithelial cells are SLIGHTLY permeable to urea.

The concentration of urea is considerably higher in the filtrate as compared to the blood
in the capillary.

Thus, urea diffuses passively through the epithelial cells of the PCT and into the blood.

Half of the urea that is present in the filtrate is reabsorbed this way.

The reabsorption of much water and solutes from the filtrate greatly reduces its volume.

Even so, in an adult human, around 125cm3 of filtrate enters the proximal convoluted
tubule.

Though every MINUTE, only 64% of this filtrate remains unabsorbed and passes onto the
loop of Henle.

Further Water Retention

In a nephron if you observe, the loops of Henle are parallel to the collecting ducts present
in the medulla.

The loops act to create a high concentration of sodium and chloride ions within the tissue
fluid of the medulla.

Remember that tissue fluid is the space between cells in a tissue or organ.

Such a buildup of concentration is partly done by active transport by the cells of the
thick region of the ascending limb of each loop.

The concentration of solute present within the tissue fluid of the medulla can be 4x more
than the concentration of solute present in the blood plasma.

The development of such a tissue fluid within the medulla causes a lot of water to go
FROM THE FLUID IN THE COLLECTING DUCT INTO THE TISSUE FLUID, this is
AS THE FLUID FLOWS THROUGH THE MEDULLA.

This water that has now entered the tissue fluid, is kept in the medulla and does not pass
along with the fluid in the collecting duct.

The kidneys as a result perform such a mechanism to retain water, instead of excreting it
with urine.

This is to prevent dehydration.

The filtrate after its departure from the loop of Henle heads into the distal convoluted
tubule, and from there it heads to the collecting duct.

As it goes into the collecting duct, it runs into the medulla AGAIN. (See above).
It passes the regions of the medulla where the solute concentration present within the
tissue fluid is high.

The water potential of such tissue fluid is very low.

Water thus moves out of the collecting duct into the tissue fluid present within the
medulla.

It moves by osmosis, and it is until the water potential of urine present in the collecting
duct is the same as the water potential of tissue fluid present within the medulla.

That water potential in the tissue MAY BE much greater than the water potential
that is present within the blood.

Hence, water can move by osmosis back into the capillaries of the blood.

Thus, the degree to which the above process occurs is controlled.

This is by the hormone, antidiuretic hormone, or ADH.

Antidiuretic hormone is a hormone secreted from the posterior pituitary gland that
increases water reabsorption in the kidneys and therefore reduces water loss in
urine.

The amount of water that is retained has a dependency on the relative thickness of
the medulla in the kidneys.

Such be the case for mammals, and we can also define the above as the ability to produce
concentrated urine.

The maximum urine concentration that is produced by humans is 4x that of the

concentration of the blood plasma.

Kangaroo rats and gerbils, which are desert rodents, can produce urine concentration
which is 20x of that of their blood plasma.

Such is possible because the cells in the medulla of these mammals are relatively large.

The cells that line the loop of Henle in these mammals have deep infolds.

This essentially increases the surface area for the pumping of ions, Na+ and Cl-.
Increase pumping would increase the steepness of the water potential gradient
between the fluid present in the collecting duct and that of the tissue fluid.

The cells in their loops also have numerous Na+-Ka+ protein pumps. (separate pumps).

There are also numerous mitochondria within the cytoplasm of these cells.

Each mitochondrion itself has many cristae, an increased surface area thus for
oxidative phosphorylation.

The cells of the loop can thus produce a lot of ATP, available to pump sodium ions into
the tissue fluid.

The distal convoluted tubule’s first part has a function like that of the ascending limb
of the loop of Henle.

The second part of the DCT acts in the same way as the collecting duct.

In the DCT and the collecting duct, sodium ions are pumped actively into the tissue
fluid from the tubule.

These ions then pass from the tissue fluid into the blood.

THOUGH, potassium ions are actively transported INTO the tubule.

The rate at which these two ions move into and out of the fluid can vary.

It is this very rate that supports the regulation of the concentration of ions within
the blood.

Sodium ions and potassium ions also serve their importance in the conduction of nerve
impulses.
Take note in the graph above, the concentration of urea, which is referred to as the
concentration of urine later, increases due to the loss of water within the nephron.

Osmoregulation is the control of water potential of bodily fluids within the body.

Such regulation is vital in the overall process of homeostasis.

It involves the hypothalamus, posterior pituitary gland (in brain), and the kidneys.

Osmoregulation is the control of the water potential of blood and tissue fluid by
controlling the water content and/or the concentration of ions, particularly sodium
ions.

For the water potential of the blood to be controlled, it needs to be monitored.

This is done with the help of special sensory neurons.

These sensory neurons are termed osmoreceptors, and they are present in the
hypothalamus.

Considering a set point, if the water potential of the blood falls below this set point, then
such change of a physiological factor is detected.

This change is sensed by receptors, in this case, our sensory neurons present in the
hypothalamus.

The impulse thus travels along the sensory neurons towards the posterior pituitary
gland.

At the pituitary gland, the osmoreceptors terminate, they finish.

The impulses stimulate the release of the hormone, antidiuretic hormone.

ADH is a peptide hormone, it is made up of 9 amino acids.

Take note IT IS NOT A polypeptide.

ADH is made to enter the blood, where it flows in the capillaries.

It has the effect of making the kidneys reabsorb as much water as possible from
urine, reducing the loss of water from the body due to the loss of urine.

The term “diuresis” means the production of dilute urine.

As we have defined ADH as ANTIdiuretic, it gets such name from the fact that it
prevents the formation of dilute urine.

This is as it stimulates the reabsorption of water.

Water is reabsorbed into the blood from the filtrate in the collecting duct of the nephron.

It does this by osmosis.

The target cells for our hormone ADH, are the cells of the collecting duct.

It acts to make them MORE PERMEABLE to water than usual.

At the luminal membranes of the cells of the collecting duct are aquaporins.

These serve as water-permeable channels, allowing the movement of water by osmosis

from the filtrate into the cells.

An increase in the permeability is brought by increasing the number of aquaporins in

the luminal membranes of the cells of the collecting duct.
Within the cells of the collecting duct are vesicles.

These vesicles withhold aquaporin channels within their membranes.

ADH molecules bind to receptor proteins which are present on the surface of the cells.

This stimulates the production of cyclic AMP, which can be also said as cAMP.

This is a secondary messenger molecule; it leads to the activation of a signaling

cascade.

Such cascade causes the eventual phosphorylation of aquaporin molecules within the
vesicles.

This leads to these molecules becoming activated, and at the activation of these
molecules, the vesicles move towards the luminal membrane of the cell.

The vesicles fuse with the luminal membrane, causing the placement of aquaporins at
its surface.

The membranes of the cells of the collecting ducts have now increased in their
permeability towards water.
In the above diagram, ADH binds to receptors present on the cell surface membranes of
the cells of the collecting duct.

This causes a series of enzyme-controlled reactions, ending with the production of an

active phosphorylated enzyme.

This enzyme causes the movement of vesicles which contain aquaporins towards the
cell surface membrane.

The vesicles fuse with the luminal membrane of the cells, and water now can move down
its potential gradient from the lumen of the collecting duct, through its cells, into the
concentrated tissue fluid, and eventually into the blood plasma within the capillaries in the
medulla of the kidney.
cAMP also acts as a second messenger in the control of the blood glucose
concentration.

As fluid now flows through the collecting duct, water molecules move through the
aquaporins present in the luminal membranes of its cells.

They move out of the tubule, and into the tissue fluid present in the medulla.

This is as the collecting duct has a higher water potential than the tissue fluid in the
medulla, and thus water moves out of the collecting duct and into the tissue fluid.

The fluid that remains in the tubule now has a lower water potential due to the loss of
water, it becomes more concentrated.

Thus, the secretion of ADH causes the increase in the reabsorption of water from the
filtrate in the nephron into the blood.

Now, a small volume of CONCENTRATED URINE flows from the kidneys, through the
ureters and into the bladder to be eventually excreted.

When you take in a lot of water, there is an increase in the water potential of the
blood.

The water potential of the blood RISES above the set point, this DOES NOT cause
the stimulation of the osmoreceptors.

ADH is secreted within the posterior pituitary gland, and as the result above the gland
stops secreting ADH.

A lack of stimulation from ADH towards the cell of the collecting duct causes
aquaporins to be moved out of the luminal membrane.
They in a reversed sense, go back into the cytoplasm becoming a part of being withheld in
the vesicles again.

The collecting duct cells are now IMPERMEABLE to water.

The fluid present within the collecting duct flows down it, and dilute urine eventually
collects in the renal pelvis.

It flows down the ureter to the bladder.

Take note the water potential is not only related to the concentration of the filtrate,
but also to its volume.

In the case of drinking large volumes of water, you produce large volumes of dilute
urine.

This is to ensure you lose much of the water you drank.

This keeps the water potential of the blood constant.

However, take notice.

The cells of the collecting duct are not able to respond immediately to the reduction
of the secretion of ADH from the PPG.

ADH present within the blood has not broken down yet, and thus, until it's broken down
the cells can't behave respective to the reduction of the stimulus.

About half of ADH that is present within the blood is broken down approximately
every 15–20-minute time interval.
Though, the time interval it takes for aquaporins to be removed from the luminal
membrane and transported to the cytoplasm of the cells is shorter.

This time interval is activated as said above, AFTER the breakdown of ADH.

It takes 10-15 minutes approximately for the aquaporins to be removed from the
luminal membrane into the cytoplasm.

Take note of the mechanism of osmoregulation in the graph above.

We have discussed that the thick region of the loop of Henle, the ascending limb
performs active transport, causing a buildup of concentration in the tissue fluid.

It does this by the active transport of ions.

Water present within the descending limb of the loop of Henle (which comes first),
moves down its potential gradient into the tissue fluid by osmosis.

This increases the concentration of fluid within the loop of Henle within the nephron.

Though, till a certain point the gradient of water potential shifts from descending limb
to tissue fluid to tissue fluid to descending limb.

The concentration of the fluid within the loop of Henle is levelled, as you can see from
the short levelling above.

The pumping action of ions from the ascending limb decreases the concentration of
the fluid present within it, and the process is repeated.

At the presence of high ADH, the collecting duct is more permeable to water.

Water thus moves down its potential gradient from the cells of the collecting duct
into the tissue fluid.

This increases the concentration of fluid present within the collecting duct in the
nephron.

In humans, we transport carbohydrate within the blood plasma as glucose in solution.

In a healthy jolly bolly person, each 100cm3 of the blood contains 80-120 mg of glucose
normally.

This is in other terms between 4.4-6.7 mmoldm-3.

We can define this close to the set point of glucose within the body.

At the decrease of concentration below such range, cells may not have sufficient glucose
available for respiration.
Consequently, the cells cannot carry out their normal activities.

Such is vital in severity in the case for brain cells, as they only respire using glucose.

At quite high concentrations of glucose above this range, the normal behavior of cells
again is disturbed.

Thus, we need appropriate hemostatic control for the concentration of glucose present
within the blood.

Such control is acted out by 2 hormones, glucagon and insulin.

These are secreted by the endocrine tissue that is present within the pancreas.

Within the tissue are groups of cells.

These are defined as the islets of Langerhans, and these cells are found throughout the
pancreas.

"islet" means a small island, such as you may find in a river.

The islets within them consist of two types of cells.

These are alpha and beta cells respectively.

Alpha cells secrete glucagon.

Beta cells secrete insulin.

The alpha and beta cells ACT AS BOTH receptors and central controls for the
hemostatic mechanism they perform.
The hormones they secrete coordinate the actions of effectors; this is why these cells
act as central controls.
Take note regarding effectors it is important to note we are not talking about the endocrine gland rather target cells which will carry out a
response to the binding of either insulin or glucagon to them.

Glucose is absorbed from the small intestine; it is absorbed into the bloodstream.

Alpha and Beta cells detect an increase in the blood glucose concentration.

They directly respond to such a change.

Alpha cells stop the secretion of glucagon and beta cells secrete insulin into the blood
plasma.

This insulin is carried to all parts within the body.

Insulin is a protein, and consequently it can’t pass directly through the cell surface
membranes of cells, stimulating appropriate mechanisms.

It instead binds to a receptor that is present within the cell surface membrane of the
cell.

Indirectly, it stimulates the cell with the support of intracellular messengers.

There are many receptors that are specific to insulin.

Such could be the those present on cells of the liver, muscle and adipose tissue.

Insulin acts to stimulate cells with the use of these receptors.

It causes an increase in the rate of absorption of glucose from the blood, and it also
causes the conversion of glucose to glycogen.

It also increases the uptake of glucose in respiration.

Its overall effect causes a decrease in the concentration of glucose in the blood.

Glucose does not just enter cells.

It enters only by facilitated diffusion, and as the word facilitate terms, it enters with
the help of special transport proteins.

These proteins are known as GLUT.

There are different types of GLUT proteins, this depends on the tissue they reside in.

Muscle cells have GLUT 4 transport proteins.

Just as aquaporins, GLUT proteins NORMALLY are kept within the cytoplasm within
vesicles.
Insulin binds to receptors present within the cell surface membranes of MUSCLE
CELLS, and such binding causes the eventual movement of such vesicles from the
cytoplasm towards the cell surface membrane.

After the fusion of the vesicles with the membrane, the GLUT 4 protein transports
facilitate the movement of glucose into the cell.

Brain cells consist of GLUT 1 proteins, and liver cells consist of GLUT 2 proteins.

BOTH OF THE ABOVE, 1 AND 2, ARE ALWAYS PRESENT AT THE CELL SURFACE
MEMBRANE AFTER THEY ARE SYNTHESIZED.

Their distribution inside the cell is NOT AFFECTED by insulin.

Insulin also stimulates the activation of the enzyme glucokinase.

It causes the phosphorylation of glucose.

Glucose has now been trapped inside the cells; this is as PHOSPHORYLATED glucose
can’t pass through the protein transports present on the cell surface membrane.
Glycogen is a large, insoluble polysaccharide molecule.

It is made by glucose monomer units; these are linked to each other by 1,4 glycosidic
bonds and 1,6 branching points also made by glycosidic bonds.

It serves as a short-term energy store, and it is found in LIVER AND MUSCLE

CELLS.

It is converted back into glucose easily.

Insulin also activates 2 other enzymes.

These are phosphofructokinase and glycogen synthase.

Together, they have a collective role in the addition of glucose molecules to glycogen in
liver and muscle cells.

They do this in a process termed glycogenesis, it causes the production of glycogen.

It is the synthesis of glycogen by the addition of glucose monomers.

Above, we can say the receptor overall, SIGNALS to the cell to cause the movement of
the vesicles to the cell surface membrane.

At the presence of the transport proteins, glucose can now diffuse down its concentration
gradient into the cell by facilitated diffusion.
In the TEM of the liver cell above, you can observe glycogen (GLY) as dark spots.

Mitochondria are also visible.

At the decrease in the concentration of glucose within the blood, the decrease is
detected by the alpha and beta cells present in the pancreas.

In response, the beta cells HAULT the secretion of insulin, and alpha cells secrete
glucagon.

The decrease in the blood glucose concentration reduces the rate of uptake or use of
glucose by liver and muscle cells.

This follows the reduction of insulin within the bloodstream.

However, uptake still persists (breakdown), though at quite a lower rate.

Take note, insulin will simply act to reduce the concentration of glucose within cells (glycogenesis), and glucagon will act to increase the
concentration of glucose within cells (gluconeogenesis and glycogenolysis).

Glucagon can bind to different receptor molecules present WITHIN the cell surface
membranes of LIVER CELLS.

Glucagon receptors ARE NOT EXISTENT IN MUSCLE CELLS.

The response to the ligand in this case, glucagon, causes the same method of cell signaling
as described above.

This follows the general understanding of cell signaling we have from chapter 4.

As a reminder.

The process of cell signaling involves the secretion of a ligand, which is a messenger
molecule.

The glycoprotein or the glycolipid on the membrane of the target cell acts as a

receptor, and it has a shape specific to that of the ligand.

The ligand binds with this receptor, causing it to change in shape.

The receptor then spans into the cell, this change in shape gives it the ability to

interact with the next molecule in the signaling pathway.

Such doing is called transduction, where a signal is now being converted into a message
that is transmitted.

The interaction with the G protein acts as a switch, this brings upon the release of

a secondary messenger molecule VIA an enzyme.

At the stimulation of JUST one receptor, numerous second messenger molecules are made
in response.

This is an example of amplification of the original signal.

The secondary messenger molecules bring upon the activation of enzymes, such enzymes

bring upon the activation of other enzymes as well.

This increases amplification at each stage, as enzymes are activated to activate further
enzymes.

The sequence of events triggered by the G protein is defined as a signaling cascade.

The activation of other enzymes occurs until the final enzyme is reached.

After the binding of glucagon with the receptor, the signal is relayed by a method of
transmission.

It has now become a message that is being transmitted.

Transduction has occurred.

As glucagon binds with the receptor, it causes a conformational change in the receptor
protein.

Such conformational change allows the receptor protein to activate a G protein inside
the cell.

This G protein in turn causes the activation of the enzyme, adenylyl cyclase.

Just as the receptor, this enzyme is part of the cell surface membrane.
Take notice, the G protein activates the enzyme, adenylyl cyclase.

This enzyme produces the second messenger molecule.

This second messenger can activate an enzyme which can also activate another enzyme,
which can activate another enzyme...and so on.

Such a cascade is an example of amplification of the signal.

- Adenylyl cyclase catalyzes the conversion of ATP to cyclic AMP or c-AMP.

This is our second messenger molecule.

- c-AMP molecules bind with protein kinase A molecules within the cytoplasm
activating them.

- Active protein kinase A molecules activate phosphorylase kinase enzymes by adding

phosphate groups to them.

- Active phosphorylase kinase molecules activate glycogen phosphorylase enzymes

with the addition of phosphate groups TO THEM.

We legit be passing phosphate groups.

The above is an example of an enzyme cascade, it has amplified the original signal from
glucagon.

AT ITS ACTIVATION, glycogen phosphorylase is our final enzyme.

It catalyzes the breakdown of glycogen to glucose.

It does this by a process termed glycogenolysis.

Such a process occurs by the removal of glucose monomers from the numerous “ends” of
glycogen molecules.

As the glucose monomers are released, the concentration of glucose within the cell
increases.

Thus, glucose moves down its concentration gradient through GLUT 2 proteins outside
of the liver cells and into the blood.

Glucagon also has its role to stimulate glucose formation from amino acids, fatty acids,
glycerol, pyruvate, and lactate.

This is by a process termed gluconeogenesis.

It legit means formation of “new glucose”.

So overall, because of glucagon secretion, the liver releases glucose to the blood.

This is extra glucose, and the blood glucose concentration increases.

As you have observed, glucagon and insulin work together in the negative feedback system.

Such a system in which the deviation of the blood glucose concentration from its set point,
brings upon appropriate actions from effectors.

This brings the blood glucose concentration back to normal.

It is imperative to note that the blood glucose concentration NEVER remains constant.

Of the reasons for this is the fact that there is a time delay between when the change in
blood glucose concentration occurs and the onset of corrective actions that correct it.

The change in the blood glucose concentration is dependent (other than external factors)
on the hormones, insulin and glucagon.

Insulin and glucagon have opposing effects on the blood glucose concentration.

It takes time for glucagon to reverse the effect of insulin in the changes of the blood
glucose concentration and vice versa.

Such time delays cause the factor within a control system to oscillate.

The factor does not stay at an absolute constant, rather it fluctuates by rising slightly
above and falling slightly below the normal “required” level.
Adrenaline also serves to increase the blood glucose concentration.

It also binds to different receptors present on the cell surface membranes on liver
cells.

It causes the same enzyme cascade within the cell that glucagon causes.

This causes the same end result, which is the breakdown of glycogen to glucose
catalyzed by glycogen phosphorylase.

Though it is vital to note a difference.

We have said that receptors for glucagon are not present in muscle cells.

This is why adrenaline also stimulates the breakdown of glycogen stores present within
muscle tissues DURING EXCERSIZE.

The glucose that is produced remains in the muscle cells, as it is needed for immediate
respiration.

Diabetes mellitus be a quite common disease.

People with such disease aren’t able to control their blood glucose concentration, allowing
it to not stay around normal limits.

The disease can develop early in life, this could be as Beta cells in the pancreas stop
secreting insulin.
Though most people develop this disease later with age.

This is as their cells FAIL TO RESPOND TO INSULIN.

The presence of glucose within urine may be an indication of diabetes.

This is as the blood glucose concentration rises above a certain value, not all the glucose
can be reabsorbed into the blood from the filtrate present in the proximal convoluted
tubule into the blood.

This value is not the set point, it is the renal threshold.

Glucose thus passes through the kidney unabsorbed back into the blood, and some of it will
be present in urine.

Simple tests over urine can be performed, this can give indications of health problems.

Such could be diabetes, though such indications should be investigated more thoroughly.

Test strips are used to investigate a range of factors present within urine.

Such factors include glucose, pH, ketones, and protein.

The test strip that serves to investigate glucose from urine contains 2 enzymes.

These are glucose oxidase and peroxidase.

Such enzymes are IMMOBOLIZED, this is at a small pad at the end of the strip.

Covering the pad of the test strip is a cellulose membrane, it only allows small
molecules from the blood to reach the enzymes (or small molecules from urine in this
case).

As the pad is immersed in urine for a period of time, at the presence of glucose the
following occurs.

- Glucose oxidase catalyzes the oxidation of glucose in a chemical reaction to gluconic

acid.

Such a reaction also produces Hydrogen Peroxide.

- Peroxidase catalyzes the reaction between hydrogen Peroxide and chromogen on

the pad (colorless chemical), this forms oxidized chromogen (brown compound) and
water.

The color of the pad that is released is matched against a color chart.
The colors of this color chart represent different concentrations of glucose.

Though the trend is, the darker the color, the more concentration of glucose present.

Glucose oxidase as the name suggests is specific to glucose only.

The test thus gives a negative result when other reducing sugars are used.

These can be fructose, lactose, and sucrose.

Thus, glucose oxidase serves as an excellent example of enzyme specificity and

immobilized enzymes.

Urine tests can’t indicate the current blood glucose concentration.

They only show whether the concentration of glucose within the blood was or was not
higher than the renal threshold.

This is also during the time period urine collects in the bladder.
This is why we make use of a biosensor to measure the blood glucose concentration.

A biosensor is a device that uses a biological material such as an enzyme to measure

the concentration of a chemical compound.

Such a device allows people with diabetes to check how well they are controlling their
blood glucose concentration.

The biosensor, like the test strips, makes use of glucose oxidase.

This enzyme is located on a recognition layer.

With the biosensor, a small sample of blood is tested.

A partially permeable membrane lies within the biosensor.

Small molecules within the plasma of the blood in the sensor pass through this membrane.

Such small molecules include glucose.

Glucose thus enters the active sites of glucose oxidase enzymes.

These enzymes catalyze reactions to produce gluconic acid and hydrogen peroxide as
explained above.

Hydrogen peroxide over here gets oxidized, this is at an electrode.

The electrode can detect the transfer of electrons.

The electron flow is proportional to the number of glucose molecules that are present
within the blood.

Electron flow is related to the current.

The biosensor amplifies the current, which is read by the meter, this produces a digital
reading.

The blood glucose concentration just like this, can be deduced in seconds.

The results can be stored electronically or sent to a doctor’s surgery.

Animals are not the only ones that need to maintain a constant internal environment.

Plants need to do this also.

An example of such could be the fact that mesophyll cells present within the leaf of a
plant require a constant supply of carbon dioxide.

This is so they can make the best use of the light energy they absorb.

They use this light energy to carry out photosynthesis.

As you know from the previous chapter, a low concentration of carbon dioxide limits the
rate of photosynthesis.

The diffusion of gases in and out of the leaf, and hence the entry of carbon dioxide is
controlled by the stomata.

A stoma is defined as an aperture (hole) that lies between two guard cells.

Though such a term is usually used to refer to the guard cells, specifically the aperture
between them.

Though we are considering the stomata, they seem quite simple.

Rather, it is the guard cells which enclose the stomata between them that are highly
specialized.

It is these guard cells that can respond to a wide range of external or environmental
stimuli.
They do this to control the internal atmosphere of the leaf.

A guard cell is a kidney-shaped epidermal cell found with another, in a pair

surrounding a stoma and controlling its opening or closure.

Stomata are distributed on leaves and flowers.

They are even distributed in GREEN STEMS.

It is typical for the lower epidermis of the leaf to have the greatest density of
stomata.

Each stomatal pore is surrounded by two guard cells.

These guard cells are elliptical (oval like) in shape.

They are often described as being shaped like kidneys.

Guard cells are much smaller than the spongy and palisade cells present in the
mesophyll tissue.

Though, these guard cells are very metabolically active.

Guard cells have the following features.

• They consist of thick cell walls FACING the air outside the leaf and FACING
towards the stomal pore.

Such outer wall has a THICK waxy cuticle and is often observed with extended ledges.

The walls that face the adjacent epidermal cells though, are MUCH THINNER.
Ledges are defined as small narrow horizontal surfaces.

• Cellulose microfibrils are arranged in bands around the guard cell.

The appearance resembles a donut with rubber bands.

• Guard cells DO NOT have plasmodesmata.

This allows no symplast pathway to occur involving guard cells.

• The cell surface membrane of guard cells is often folded, it contains many
channels and carrier proteins within it.
 • The cytoplasm of guard cells has a high density of CHLOROPLASTS and
MITOCHONDRIA.

• The chloroplasts which are in high density in the guard cell have thylakoids,
though unlike the chloroplasts of mesophyll they have few grana.

Such space is used to facilitate starch grains within the stroma, these increase in size
as starch is stored at night.

They decrease in size as starch is made of use in the day.

• The mitochondria of guard cells have many cristae (inner membrane fold).
 • Though the nucleus in guard cells is relatively similar in size to nuclei in
mesophyll cells, the nucleus of guard cells occupy a quite larger proportion of
the cell.

This is as guard cells are much smaller than mesophyll cells.

• Rather than 1 large vacuole, guard cells are made up of several small vacuoles.

Stomata have daily rhythms of opening and closing.

Such practices of the stomata are controlled by their respective guard cells that surround
them.
These open and close rhythms occur even when the plant is kept in constant dark or
constant light.

During the day, the opening that occurs helps to maintain the inward diffusion of carbon
dioxide and the outward diffusion of oxygen.

The outward diffusion of water vapor is also allowed with such opening.

At night, when photosynthesis can’t occur the closure of the stomata allows the
conservation of water and reduced rate of transpiration.

Stomata are not time based; they do not necessarily open in the day and close at night.

The opening and closing rhythm of the stomata is not only dependent on light intensity
(day) or darkness (night), these are not the only 2 environmental stimuli.

Such explains why stomata persist in their daily rhythm of opening and closing in constant
dark and constant light.

This is as there are other changes in environmental conditions, other stimuli which
influence the opening and closing of the stomata.
Stomata open in response to,

• Increasing light intensity.

• Low CO2 concentration within the air spaces in the leaf.

When the stomata open, the leaves gain CO2 for photosynthesis, but they lose water by
transpiration as shown above.

Take note that opening or closing will have the same consequence, regardless of the
stimulus.

Stomata close in response to,

• Darkness.

• High CO2 concentration within air spaces within the leaf.

• Low humidity

• High Temperature

• Water Stress

Such occurs when there is a limited supply of water from the roots.
It can also be due to a high rate of transpiration.

As we have made clear, the stomata can close during daylight too.

This can be due to other environmental stimuli.

A disadvantage of closing during the day is that the supply of carbon dioxide
decreases.

The rate of photosynthesis decreases.

Though the advantage of such closing is that water is retained within the leaf, such is
important in times of water stress.

The stomata open by mechanisms.

Guard cells open when they increase in water potential, becoming turgid.

They close when they decrease in water potential till, they become flaccid.
The guard cells gain and lose water by osmosis.

Take note, though the above image shows many stomata closing at night, this will not
always be the case.

It is recommended you see the book for further reference, page 387.
For the guard cells to open, we need water to enter the cells by osmosis.

The water potential of the cells needs to decrease.

Such is done by the activities of transport proteins which are present on the cell
surface membranes of guard cells.

In the response to light, the protein transports act as protein pumps.

They are powered by ATP.

These pumps in the membrane actively transport H+ ions out of the guard cells.

Such a decrease in the concentration of H+ ions in the guard cell causes

the opening of protein channels presents within the cell surface membrane.

These protein channels facilitate the movement of K+ ions into the cell.

The movement of potassium ions inside the cell is due to the cell being negatively
charged relative to its outside.

This is as it had emitted positive hydrogen ions.

Since these K+ ions have a positive charge, they move down an electrical gradient.

This gradient is towards the negatively charged region, the cell.

However, this is not the only gradient.

The K+ ions also diffuse into their cell down their concentration gradient.

We term such combined gradient an ELECTRO CHEMICAL GRADIENT.

It is not only K+ ions that enter the cell to maintain electrical balance.
Chloride and nitrate ions are also involved.

An electrochemical gradient is a gradient across a cell surface membrane that

involves both a difference in concentrations of ions and a potential difference.

The movement of such extra potassium ions inside the cell increases the overall solute
concentration in the guard cell.

This decreases the water potential of the guard cell.

A water potential gradient is thus established between the outside and inside of the
cell.

Water moves into the guard cells, through aquaporins which are present on their
membranes.

Most of this water enters the vacuoles, which increases them in size.

The turgor pressure (from turgid) of the guard cell hence increases.

The stoma opens.

Starch also plays a part in the opening of guard cells.

It breaks down in the stroma of the chloroplast of the guard cell, this forms
negatively charged malate ions.

These ions enter the vacuoles of guard cells.

They play their role in maintaining electrical balance AND decreasing the water
potential during the opening of the stoma.
Water enters guard cells to increase turgor pressure in the vacuoles.

This pressure causes these cells to expand.

Such cell expansion determines the opening or closing of the guard cells.

Guard cells have unevenly thickened cell walls.

The wall further away from the pore is thin.

The wall that is adjacent (next to) the pore is thick.

The bundles of cellulose fibers that are present within these walls, prevent expansion
in all directions.

This means that instead of the cells increasing in diameter, they increase in length.
As these guard cells increase in length, the thin outer walls of the guard cells increase
in length more readily than the thick inner walls adjacent to the pore.

This causes the guard cells to become curved.

The cells bulge (extend) into cells that lie next to them.

These are defined as adjoining cells.

They look now more like a pair of bananas when they are open than a pair of kidneys when
they are closed.

An increase in the length of the guard cell due to turgor pressure due to water opens the
pore between the cells.

Stomata close at the halt of hydrogen ion protein pumps.

Because of this, potassium ions leave the guard cells, going into neighboring cells.

Malate ions get returned to the chloroplast, where they get converted back into
starch.

A water potential gradient now occurs in the opposite direction, higher in the guard
cells and lower on the outside.

Water leaves the guard cells by osmosis.

The cells become flaccid, and the stoma closes.

Closing the stomata reduces the uptake of carbon dioxide.

It also reduces the rate of transpiration.

Transpiration can be necessary to not only cool the plant, but the maintenance of the
transpiration stream which provides water and mineral ions to the plant.

Stomatal closure would thus only occur when reducing the loss of water from the plant or
conserving water supply is the priority or most important factor.

We define such circumstances as water stress, when the plant really needs to conserve
its water supply.

In such conditions, abscisic acid is produced.

ABA is a hormone produced in plants which acts to stimulate stomatal closure.

Abscisic acid is an inhibitory plant growth regulator that causes closure of stomata in
dry conditions.

ABA can be found in a wide variety of plants.

This variety includes ferns, mosses, and even flowering plants.

The hormone can be found in all areas of the plant.

It is made by all cells which have either chloroplasts or amyloplasts.

Amyloplasts are organelles which are like chloroplasts, though they have large starch
grains and no chlorophyll.

ABA serves one of its roles in the coordination of the responses to stress.

It is known as a stress hormone.

A plant responds to being subjected to difficult environments by secreting ABA.

Such environments can involve very high temperatures or reduced water supplies.

During a drought, when the water potential of a plant is in short supply, the concentration
of ABA that is present in the leaves can rise to 40x its normal.

Such a high concentration would stimulate the stomata to close, reducing the loss of water
from the leaves of the plant.

At the application of ABA, stomata close within minutes.

It seems that there are ABA receptors which are present on guard cells.

At the possible binding of ABA to these receptors, the protein pumps which are
responsible for the pumping of hydrogen ions are inhibited.

ABA also acts to stimulate the movement of calcium ions into the cytoplasm of the
guard cell through its cell surface membrane and into its vacuole through its tonoplast.

These calcium ions act as second messengers.

They activate channel proteins which permit the movement of negatively charged ions
outside the guard cells.

This in turn causes the opening of more channel proteins (amplification).

Such protein channels cause the movement of potassium ions outside of the guard
cells.

AT THE SAME TIME, the calcium second messengers stimulate the closure of channel
proteins.

These channel proteins ALLOW the movement of potassium ions into the guard cell
(via a concentration gradient).

The loss of ions increases the water potential of the guard cells.

Water passes out of the cells by osmosis, and the guard cells become flaccid.

They close.