7/4/2011 3:57:00 AM

Physiology Lecture 23

Principles of countercurrent multiplication and exchange,

this is how the kidney forms a concentrated or dilute
urine. We had talked about last week when we looked at
bp regulation how ADH was involved in changing water
permeability properties of the collecting duct. And so
when ADH was around that opened up aquaporin
channels produced more aquaporin channels in the
princilpal cells of the collecting duct so water could leave
the tubular fluid within the collecting duct and go into the
interstitial space, be absorbed by the vasa recta and
carried back to the body. So our question today is how
does that water reabsorption occur, why does water
leave the collecting duct. Were going have to look at
the anatomical and functional relationships btwn the loop
of henle, collecting duct, and the vasa recta.

So 1st were going to look at what osm and volume

changes occur along the renal tubule. When ADH is
around?
Loop of Henle and collecting duct work together to form a
concentrated urine, or establish the environment to do
that.
Diff btwn countercurrent multiplication which is the thing
that happens w/ loop of henle, and countercurrent
exchange which is something that happens w/ the vasa
recta.
Finally well look at things that may alter your ability to
form a concentrated urine.

So.

We have the outer section of kidney cortex, proximal

tubule, distal, and parts of the collecting duct. Then we

have a medullary portion deeper inside kidney: loop of

henle, medullary portion of the collecting duct.

Insterstitial osmolarity it starts out at around 300. It

starts out at 300 in the cortex of the kidney, the
instersituium is that space that surrounds the cells but its
not within the blood vessel, space btwn cells and bvs.

600

1200

Osmolarity of that insterstitial space changes from being

isotonic in the cortex to hypertonic down at the base of
the loop of henle.

These diagrams in physiology and histology are

misleadingthese tubules are packed together (handful
of pens).
If you look at ends of these, there is space in btwn each
of these tubes, and thats the interstitial space. Tightly
packed, IS surrounds every one of these tubules.

See thin ascending , thin descending, collecting duct,

depending on section.
Packed real close together, so numbers are the same
everywhere (osm numbers).
Fluid coming in from glomerular capillary is essentially
isotonic w/ blood and so the Na , K , bi carb , etc
Concentrations are the same as in tubular fluid as in
glomerulary capillary. Through a variety of Na
cotransport, countertransport processes, Na is
reabsorbed and because the proximal tubule is very
permeable to water, water follows. And out here is the

peritubular capillary bed , osmotic oncotic and

hydrostatic pressure within this peritubular bed favored
continued water reabsorption, so water leaves and goes
into IS. So even though tubular fluid and intersitium have
the same osmolarity its because water and salts are
drawn into the blood because of that balance of starling
forces where oncotic pressure here in the peritubular cap
bed was greater than hydrostatic, and that led to water
and salt reabsorption. So liquid leaving the proximal
tubule and going into the descending limb is isotonic,
even though a large proportion 60-70 percent of
everything that gets filtered got reabsorbed in the
proximal tubule, but its reabsorbed isotonically salt and
water go together. So even though the volume is much
smaller thats coming into the descending limb, its still
300mosm. As fluid goes down the descending limb, the
tonicity of the tubular fluid increases, and becomes equal

to whatever it is in the Intersititium. The descending limb

is permeable to water, but not permeable to salt. ***

By the time that liquid reaches the loop, the bottom of

the loop, it has equilibrated with whatever the Intersitital
osm is , and so this tubular fluid as shown in this diagram
is around 1200mosm, 4 times as concenctrated as blood.

As this tubular fluid goes back up again the ascending

limb, the thin ascending is permeable to salt, so salt can
leave, but also and even more importantly the
tritransporter is located in the thick ascending limb. This
tritransporter important in establishing this osmotic
gradient within the intersitium.

Net effect is that the combined reabsorption of Na in the

thin ascending and the thick ascending leads to a fluid
that is leaving the thick ascending limb, that fluid is

hypotonic to blood. Weve taken out a lot of salt and left

behind liquid so that now that tubular fluid is hypotonic.
This is the tubular fluid that the MD monitors , its at the
end of thick ascending limb, at the beginning of the distal
tubule. This is the fluid that the MD is monitoring.
As this fluid goes through the distal tubule, Na is
reabsorbed through the Na Cl cotransporter and very
little water can follow and so the fluid will become even
more dilute. Fig 28-4. Thats not whats shown in this
diagram, this diagram is showing what happens if there is
ADH around.
Because ADH is around there will some water
reabsorption and so this fluid becomes a little more
concentrated by the time it gets to the end of the distal
tubule and begins to go into the collecting duct. And then
as that fluid moves down the collecting duct, water and
things like urea are reabsorbed so that the fluid thats
leaving now approaches the intersitial osmolarity and you

then make in the case of ADH being around a

concentrated low volume urine. If ADH was not around
then these segments will not be permeable to water and
so this dilute fluid coming from the distal tubule will then
just flow down through the collecting duct and leave as a
dilute high volume urine. And so adjusting the properties
of this collecting duct are important for causing you to be
able to form a concentrated urine.

Anohter way to look at what we talked about , it gives us

a more quantitative view on things. Where things happen
and where it doesnt happen.

Fig 28-7
On x axis we see diff pieces of Nephron and the urine,
from the proximal all the way to collecting duct , and
then finally ending up at the urine. X axis where we
are.

Y axis- the osmolarity of the fluid. We have two lines.

Top mountain w/ ADH

Bottom line w/o ADH

Helping us see where ADH has an impact.

We have some numbers here. Mls that are being filtered

in one minute.

Normal GFR = 125 mls/ min. Thats where that 125

comes from , as fluid enters the proximal tubule, its
coming in at 125 mls or 125ml/min. By the time it
leaves, thers only 44 mls left. This is our 60-70 percent
that has been reabsorbed, 125ml down to 44ml.
Notice 2 things: the tonicity has not changed along that
proximal tubule so that one more time emphasizes that

that fluid reabsorption is isotonic. Yes, we reabsorbed a

lot of liquid over 80mls every minute, but it was
reabsorbed isotonically. The largest amount of water and
salt reabsorption is occurring in the proximal tubule, ADH
doesnt do anything there. Whether you have ADH
around or whtehter you dont have ADH around the
largest amound of water reabsoprtion is occurring in the
proximal tubule, ADH has no effect on the proximal
tubule and so it cant make it more than 60-70 percent,
that proximal tubule is so permeable to water, so
dependent on Na reabsorption, that ADH doesnt do
anything here. So even w/ ADH around we are still
reabsorbing 60-70 percent of that fluid.
Lets follow line w/o ADH.

Now we come to the loop of henle and we see that as we

descend (dont get confused because curve is going up)
we are descending going down the descending limb of

the loop of henle, water is reabsorbed along that tubule,

so water is leaving ,so therefore since salt cant follow
the osmolarity is getting higher. Thats why we went from
300 up to a little over 600 (w/o ADH). And the number at
the peak should be 25ml, so we reabsorbed some more
water along this portion of the loop of henle, along the
descending limb. Now the ascending limb is where the tri
transporter is located and so the ascending limb is
removing salt and therefore the tonicity falls, it becomes
hypotonic and in fact you can see that it becomes more
dilute than blood. Tonicity looks like it goes around
100mosm/L , to a 1/3 of what blood is. Because water
cant follow that salt the tubular volume remains the
same, still 25ml. Water went out along the descending
limb, salt went out along the ascending limb and so we
end up w/ a smaller volume, so the loop has absorbed
19ml around of water, so another 25 percent or so has
been reabsorbed in the loop of henle.

So now this fluid continues, its dilute, continues through

distal tubule collecting duct, and if there is no ADH
around there is no opportunity for water to be
reabsorbed since the principal cells dont have aquaporin
channels in them unless there is ADH around, so that
fluid remains relatively hypotonic and maybe a little
water gets reabsorbed here in the early portion of the
distal tubule but generally we have a high voume dilute
urine in the absence of ADH.

Now lets add ADH, again ADH does nothing to the

proximal tubule so it reabsorbs its normal amount, one of
the ***ADH does it to stimulate the tritransporter, what
that does is causes the tritransporter to put more salt
into the interstitial space and increases the osmolarity of
the IS. And you can see that our max osmolarity has
gone to 1200 from where it was before (over 600), thats

because that tritransporter amongs other things has put

in more salt, so consequently as liquid descends the thin
descending limb more water is reabsorbed, and the
tonicity approaches that in the deep medulla of the
kidney, and then along the ascending limb, we see the
tritransporter is removing that salt from the tubular fluid,
putting into the IS, and again our tonicity comes down
and is still hypotonic in the distal tubule even though
ADH is around because these portions in terms of water
permeability are unaffected or affected little by ADH
(early distal tubule, little change). So as we get to the
late distal tubule, that tubule is able to reabsorb water
and so we see the tonicity change as we go from
hypotonic to isotonic over this segment. This is affected
by ADH we got a hypotonic fluid in the distal tubule, it is
then being drawn out by the isotonic fluid in the
intersitium and we reabsorb from 25ml up to 8ml at the
end of that cortico portion of the the collecting tubule, so

a lot of water from 25ml to 8ml , we reabsorbed in the

presence of ADH another 17ml /min in the late distal and
early collecting ducts that are up at the cortex, So
another big piece of water reabsorption occurring there
when ADH is around.
Now this small volume of tubular fluid that is isotonic is
moving through the portion of the collecting duct that
goes through the medulla , through the deeper portions
of the kidney where the intersititial fluid is now
hypertonic, and so in the presence of ADH those principal
cells in the medullary collecting duct are permeable to
water, so water leaves, and we get even more
concentrated urine (high osmolarity) that is of even a
smaller volume (.2ml).

So now weve reabsorbed all but .2ml of that fluid that

was left, so the final urine volume will be small and the
tonicity will be high.

In the presence or absence of ADH, lot of water

reabsorbe in the proximal tubule.
In the presence of ADH, we get enhanced water
reabsorption along the descending limb of the loop of
henle, we get enhanced water reabsorption in the late
distal and the cortico collectin duct, and we get enhanced
water reabsorption in the medullary collecting duct.

So proximal tubule reabsorbs the largest amount ,

followed by the descending limb of the loop of henle,
then the late distal cortico collecting duct, and finally the
medullary collecting duct tops things off.

Proximal tubule bigger than any other areas for

reabsorption of water.

Fig 38-17

Understand why numbers change.

Several things happen simulatenously, well discuss one

at a time.

We got some things that influence and help us make this

osmotic gradient. Our goal is to explain how we have this
gradient in osmolarity starting close to isotonic near the
top portion of the medullary collecting duct or loop of
henle, and how it gets more concentrated in the
intersititum at the tip.

One, is the structure , these are things that are important

for generating this osmotic gradient.
1. Structure, you have to have a loop, lf you dont have a
loop you cant make this happen.

Length loop and length of loop. The longer the loop, the
bigger the gradient you can make. Desert rats that get all
water from nuts, have very long loops of henle.
Body cannot adjust length. We have a fixed loop length
but length is imp.
2. Flow fluid is always moving through the tubular fluid,
through the loop of henle, so that constant flow of fluid is
important in helping to establish the gradient. And you
know from autoregulation that the kidney tries to keep
GFR fairly constant , so that fluid movement through the
tubules is relatively constant so that enables then the
loop of henle to have just a constant flow of fluid so the
flow is imp.
3. Permeability properties-so the descending limbs of the
loop of henle, have a different water and salt
permeability than the ascending limb, descending
permeable to water, not to salt. Ascending permeable
to salt, not to water. That diff in perm prop imp.

4. Tritransporter responsible for the initital event, the

primary action that then enables all other things to occur
subsequently.

Structure fixed
Perm fairly fixed
Flow isnt
Tritransporter- well talk about how it works.

Loop A
Here we have the thin descending limb and the thick
ascending limb, and we have in middle and all over the
medullary instersitium.
We start out with tubular fluid coming from the proximal
tubule filling the loop of henle, and that fluid is isotonic.
300 everywhere. And 300 in the MI. Initial position.

The tritransporter located on the asencding thick limb,

pumps salt out of the tubular fluid and puts it into the
intersititium. That tritransporter pumps until there is a
difference in conc. of 200mosm. It is able to establish
that difference, if the intersititum becomes bigger than
that 200 diff, that means some salt will go back in other
direction and the tritransporter will try to kick it out ,
were in a steady state btwn what can come back and
what it can pump against, but it can establish a diff of
200mosm.
If we just start w/ first line , we see that this 300 btwn
the tubular fluid in the ascending limb and the I. So the
tritransporter can make this becomes 200 different so we
get that here (1st line B). But as soon as this osm begins
to go up, then water will leave the fluid in the thin
descending which will dilute this a little bit which will
mean the tritransporter will pump out some more salt,
which will mean some water will leave from the

descending limb , and finally we reach a condition where

were in some kind of steady state w/ a 200mosm diff
across the ascending limb and equality across the
descending limb. And since we have 300 all through
here, we will have the same situation once weve reached
a steady state. Important thing was we had this
tritransporter that could establish that gradient, water
couldnt follow, so the permeability propoerties of the
ascending limb help that to establish that osmotic
gradient and then the water perm of the descending
enable the descending tubular fluid to equilibrate w/ I
fluid. We still havent made a gradient.

So nothing stays the same , changes, so tubular fluid

comes in from proximal tubule, Now we have fluid
entering and so we have little boxes coming in at 300
displacing the boxes that were at 400. That moves the
stuff around and pushes these guys up at the other side,

and so the tritransporters says I dont have a 200

gradient, its only 100 , so it pumps and estabilishes a
200mosm diff btwn 2 sides, and now the fluid in the
descending limb leaves to try to make equilibration and
we start seeing 500 in the bottom and 350 top. So a little
bit of introduction of fluid displaced relationships btwn IF
and tritransporter responsible for establishing this
gradient, so flow is imp because it looks like bringing in
new fluid thats isotonic upsets the balance which makes
us pump some more it has displaced fluid that was a little
hypertonic into an area where its even more hypertonic
and this and the tritransporter keeps that gradient going.
So now we have a new steady state, I is 350 at the top ,
500 near the tip , we see the descending limb is
hypertonic ascending limb is hypotonic as it goes towards
the top ,and this fluid is hypotonic and will be going on to
the distal tubule. So one more time, we get some more
isotonic fluid from the proximal tubule, it equilibrates

with the IF, water leaves diluting IF, we no longer have a

200 mosm gradient across the wall of the thick ascending
so the tritransporter kicks in , establishes this gradient,
fluid in the descending limb equilibrates and it looks as
though were making an even bigger gradient now were
at 325, 600 at the tip (Diag F). We introduce a little more
fluid, pushes everyone around and as last chart implies
we can then generate situation where we can get a nice
steep gradient through the action of fluid flowing through
the loop, the different permeability properties btwn the
des and as limb as well as action of tritransporter to be
able to establish and maintain a concentration gradient
across the walls of the thick ascending limb, so thats
how the Intersitial gradient is established through these
things. Now the purpose then of the loop of henle is to
make that gradient, the liquid thats leaving is hypotonic
all the time, so the loop of henle isnt concentrating the
urine , its in fact diluting the urine , and that salt that has

left that fluid is being put in the I space, and the next
step willl be the use of that fluid, or osmotic gradient to
reabsorb water and thats where the collecting duct
comes in. So collecting duct passing through the same
area where its 312 at top and 700 at bottom. So here is
our dilute fluid going down the collecting duct, so the
collecting duct is passing through this medullary area
where there is this high osmotic intersitium, and if there
is ADH around water can leave and therefore lead to a
small volume concentrated urine. So the collecting duct
within the medulla makes use of the osmotic gradient
that the loop of henle generated. So again the structures,
the relationship btwn the loop, the intersititum, and these
medullary collecting ducts is important, so the loop
makes the gradient , the collecting duct uses the gradient
in the presence of ADH.

Understand Process. What things are impo to make

gradient, which structure makes gradient, how this
gradient used by other struct.
Multiplication because it got bigger
Countercurrent flow going in two diff directions

Countercurrent multiplication is what happens w/ the

loop of henle and the intersitium, countercurrent
exchange is what happens in the vasa recta.

So back in this diagram we had loop and collecting duct,

we also have vasa recta, other capillary bed that supplies
nutrients and removes waste and salts and water from
this meudllary area.

Diag 38-18

We see that intersitium is here around 1200 at the tip

and is some 300 in the cortex.

We need to supply those epithelial cells of the loop of

henle and of the collecting duct w/ nutrients and we
need to take away their waste, we have blood that we
know is isotonic 300mosm, so how can we bring this
liquid blood into the area around the loop of henle (tip)
and collecting duct, have a capillary bed where things
freely exchange back and forth and not wash away that
salt.

So if we had a BV coming in straight in here at 300 and

there was exchange w/ this hypertonic fluid, the
bloodleaving will be 1200mosm, and the capillaries will
provide nutrients but the poor ascending limb worked so
hard to establish this osmotic gradient, and now were

bringing blood in thats going to wash away that gradient

and take it back to the body , we need a process that
prevents that or minimizes it.
So again we use a loop, countercurrent relationship here.
So blood is coming in into vasa recta at 300, this is now a
capillary bed so its freely permeable to salt and water
and so as the blood passes down the descending portion
of the vasa recta moving into the tip of the loop of henle,
it equilibrates , salt and water move appropriately, it
equilibrates w/ the intersitium. And so as this diag
implies, it reaches the same tonicity as the intersitium, if
this blood were now to leave from the medulla of the
kidney it will carry blood away at 1200 mosm but instead
it goes back up the ascending side of the vasa recta and
the opposite happens salt and water requilibrate and the
blood now leaving and going into a vein is now slightly
hypertonic (325) but certainly not as hypertonic as it had
been down at the tip, so this countercurrent exchange

because all were doing is exchanging salt and water,

enables us to perfuse deep within the medulla, perfuse
w/ blood structures deep within the medulla, w/o
removing very much salt. Yes, a little bit of salt left, so
its a little hypertonic, but not as bad as it could have
been.
So thats countercurrent exchange which is the process
used by the vasculature to provide perfusion w/o washing
the salt away. Same structure in skin. Not unique to
kidney, but imp because it enables perfusion of
structures w/o loss of salt.

If we were to increase blood flow, then this exchange will

not be as complete because all of the movements require
time. So more salt will be lost. Increase blood flow =
causes increased salt lost from the medullary I.
Increased blood flow would be detrimental to producing a
low volume urine because w/ increased blood flow more

salt will be washed away , the I will not be at 1200, will

be less, and so body couldnt reabsorb as much water.
The times that we have increased blood flow, such as
increased MAP, is just the right time we want to make
more urine. If we have an increase in MAP, one way to
lower and bring MAP back to normal is to make more
urine. Increasing vasa recta bloodflow will wash away
some of those salts, reduce the osmotic gradient from
the cortex to the medulla within the I, and therefore
reduce how much water gets reabsorbed so that will go
into urine and be lost from the body , and help bring bp
down. When we have a fall in MAP, we reduce vasa recta
bloodflow, that enables less salt to be removed, therefore
helps to concentrate urine better.
So loop of henle responsible for the gradient, collecting
duct makes use of that gradient, the process within the
loop of henle that generates that gradient is
countercurrent multiplication, requires different

permeability properties btwn asc and desc limbs to salt

and water, requires the loop config, requires flow, and
requires the tritransporter.
The vasa recta also organized in loop config in order to
perfuse but not wash out too much salt. So we have
countercurrent exchange rather than countercurrent
multiplication.

Tritransporter always working so always on osmotic

gradient in MI, ADH just makes it go faster, always
pumping along.
One more thing,

Urea is the way body gets rid of N, not a toxic subs, just
a way the body combines a couple of Ns and excretes it.
Urea has interesting properties, but it also plays imp role
in helping to increase the osm here in the I. Other thing,
its movement across cell membranes is sensitive to ADH,

so its also regulated by ADH. So this little diagram vasa

recta coming in, loop of henle, collecting duct, close
together.
Numbers in tubule represent the percent of urea that is
starting, we start w/ 100 percent of urea. We filter urea,
urea is freely permeable through cell membranes ,unless
theyre not. 300mosm solution of urea is isoosmotic but
not isotonic, because for most cells urea is clearly
permeable. So we filter Urea so 100 percent or the same
conc of urea thats in the blood enters the proximal
tubule , and as that fluid passes through the proximal
tubule, half of the urea is reabsorbed , just through
channels, passively. That fluid then stays 50 percent, so
not much urea leaves during the descending limb and in
fact, urea is actually added back to the tubular fluid on
the ascending limb, such that the fluid leaving the
ascending limb actually has more urea in it than the fluid
that entered the proximal tubule , so if you add those

numbers 60 (from collecting duct) +50 =110, this diag

showing us that 60 percent more urea is added by
secretion in the asc limb of LH, which then makes the
urea conc greater in the tubular fluid than it was in the
proximal tubule. From here on, through the distal tubule
and the cortico collecting ducts these cells are
impermeable to urea. So urea cant leave , and you know
water and stuff move back and forth. So fluid coming into
the medullary collecting duct has a high urea
concentration. In the cortico collecting duct and late
distal, water could be reabsorbed so that would help to
further concentrate the urea. So the urea conc entering
the medullary collecting duct is high. What happens as it
passes down the collecting duct, is this portion of the
collecting duct is now permeable to urea and is even
more permeable if ADH is around. So because the urea
conc in this tubular fluid is high relative to the I, urea
leaves and that high urea conc. in the I is what is

enabling the secretion of urea into this ascending limb so

we generate a gradient for urea to go from the medullary
collecting duct fluid into the I , from the I into the
ascending limb and so some of the urea essentially just
cycles it reeneters the tubular fluid in the ascending limb,
gets concentrated as it passes along the distal and
cortico collecting duct and then is reabsorbed in the
medullary collecting to be re secreted into the thin
ascending limb. Some of it a little bit also gets taken up
by the vasa recta and returned to the body. So theres a
urea cycle here that enables secretion , reabsorption to
occur through this medullary area of the kidney. When
urea leaves water follows. ( HELPS US CONCENTRATE
URINE) The two of them go together, what happens then
is the osmolarity here is diluted a little by that water that
has left the collecting duct w/ urea which enables more
Na Cl , its diluting the osmolarity , which enables Na CL
to be added from the thin ascending through a passive

process and helps to add osmotic particles to this MI

fluid. So the presence or the movement of urea and
water out of the collecting duct dilutes some of this
osmolarity enhancing Na CL reabsorption from the thin
asending that helps to put more salt there to further
enhance water reabsorption and this is enhanced further
by ADH, so ADH increases water permeability and
increases movement of Urea into that space. Which is
then able to draw Na and Cl from the thin asc limb and
keep the osmolarity high and further enable water
reabsorption, if that didnt occur we wouldnt get this
additional Salt being added and the concentrating ability
will be impaired.
So this an example of a molecule that is moving back and
forth both reab, secretion, just through passive
properties. But urea there plays an important role in
helping us form a conc. urine.

Factors

Things that will limit your ability to form a concentrated

urine or to make a small volume urine.
1. Obviously the presence of absence of ADH.
In the absence of ADH, the tritransporter doesnt work as
hard, the late distal and collecting ducts are not
permeable to water, and so the fluid that is leaving the
distal tubule is hypotonic and it stays that way as it goes
down thorough the late distal and into the collecting
ducts. In the absence of ADH, there is little water
reabsorption large volume urine. This could be because
ADH isnt released from hypothalamus or it could be
because ADH doesnt work properly on receptors. No
release, or it cant work effectively.
2. Another thing that will affect ability to form a
concentrated urine is the activity of the tritransporter. A
lot of diuretics act here, the most potent ones are loop

diuretics, and they inhibit the tritransporter which means

that this osmotic graient cannot be established LH cannot
do whats its supposed to do, and so you lose salt and
water because of that.

3. Vasa recta blood flow. We talked about vasa blood flow

and how that blood leaving that vasa recta is slightly
hypertonic and so if that bloodflow goes higher then
more salt will be lost, generally the vasa recta bloodflow
is relatively small, but it can be regulated under
conditions where we want to conserve water, or where
we want to remove water.

4. Increased tubular flow. The faster the fluid flows

through those tubules , from descending through
ascending the less were able to form a concentrated
urine. Time is important, the tritransporter has to move
those molecules , the fluid in the descending limb has to

equilibrate w/ whatever the osm is in the MI, so if the

fluid is moving through those tubules too rapidly , those
gradients cant get established , therefore osmotic
gradient in the I is reduced, and thats one of the things
that a diuretic does, it causes more tubular flow, so if we
had a diuretic that acted in the loop then that would
increase loop flow, if we had a diuretic that worked even
further proximal, in the proximal tubule by increasing the
tubular flow will reduce the osmotic gradient and that will
affect the ability to form a concentrated urine.
5. Increased in GFR will push more fluid through there at
a faster rate, so increases in MAP will increasse GFR
because of an increase in glomerula capillary pressure so
more fluid will filter through, high tubular flow rate will
mean less time to form that gradient and will make a
dilute urine.
6. If we have any molecules that act as osmotic agents ,
glucose generally gets reabsorbed completely in the

proximal tubule by that transport process, Na Glucose

cotransporter, which has Tm , transporter maximum, but
if that transport max is exceeded, then glucose is left in
the tubular fluid, it doesnt get reabsorbed in later
portions such as in collecting duct or late distal, so its
holding water , that water only trying to equilbrate w/ I.
If the tubular already hypertonic because lot of glucose
there, then that equilibration wont be as thorough and so
any osmotic particles will be to increase urine formation
which is called osmotic diuresis.

7/4/2011 3:57:00 AM

7/4/2011 3:57:00 AM