Maintenance of the Body
Figure 25.17
shows the body’s response to either over-
hydration or dehydration and ADH’s role in controlling the
production of dilute or concentrated urine. When we are over-
hydrated, ADH production decreases and the osmolality of
urine falls as low as 100 mOsm. If aldosterone (not shown) is
present, the DCT and collecting duct cells can remove Na
selected other ions from the filtrate, making the urine that en-
ters the renal pelvis even more dilute. ±e osmolality of urine
can plunge as low as 50 mOsm, about one-sixth the concentra-
tion of glomerular filtrate or blood plasma.
When we are dehydrated, the posterior pituitary releases
large amounts of ADH and the solute concentration of urine
may rise as high as 1200 mOsm, the concentration of interstitial
fluid in the deepest part of the medulla. With maximal ADH
secretion, up to 99% of the water in the filtrate is reabsorbed
and returned to the blood, and only half a liter per day of highly
concentrated urine is excreted. ±e ability of our kidneys to pro-
duce such concentrated urine is critically tied to our ability to
survive without water.
Urea Recycling and the Medullary Osmotic Gradient
We’re not quite done yet. ±ere’s one last piece of the puzzle leF—
urea. We usually think of urea as simply a metabolic waste prod-
uct, but conserving water is so important that the kidneys actually
use urea to help form the medullary gradient (²igure 25.17).
Urea enters the filtrate by facilitated diffusion in the as-
cending thin limb of the nephron loop.
As the filtrate moves on, the cortical collecting duct usu-
ally reabsorbs water, leaving urea behind.
When filtrate reaches the portion of the collecting duct in
the deep medullary region, urea, now highly concentrated,
moves by facilitated diffusion out of the tubule into the
interstitial fluid of the medulla. ±ese movements of urea
form a pool of urea that recycles back into the ascending
thin limb of the nephron loop and contributes substan-
tially to the high osmolality in the medulla.
Antidiuretic hormone enhances urea transport out of the
medullary collecting duct. When ADH is present, it increases
urea recycling and strengthens the medullary osmotic gradient,
allowing more concentrated urine to be formed.
±ere are several types of
, chemicals that enhance uri-
nary output. Alcohol, essentially a sedative, encourages diuresis
by inhibiting release of ADH. Other diuretics increase urine
flow by inhibiting Na
reabsorption and the obligatory water
reabsorption that normally follows. Examples include many
drugs prescribed for hypertension or the edema of congestive
heart failure. Most diuretics inhibit Na
-associated symporters.
“Loop diuretics” [like furosemide (Lasix)] are powerful because
they inhibit formation of the medullary gradient by acting at the
ascending limb of the nephron loop. ±iazides are less potent
and act at the DCT. An
osmotic diuretic
is a substance that is not
reabsorbed and that carries water out with it (for example, the
high blood glucose levels of a diabetes mellitus patient).
The Countercurrent Multiplier
Take some time to study the mechanism of the countercurrent
multiplier in ²igure 25.16a. ±e countercurrent multiplier de-
pends on actively transporting solutes out of the ascending limb
(“Start” of the positive feedback cycle).
Although the two limbs of the nephron loop are not in
direct contact with each other, they are close enough to in-
fluence each other’s exchanges with the interstitial fluid they
share. ±e more NaCl the ascending limb extrudes, the more
water diffuses out of the descending limb and the saltier the
filtrate in the descending limb becomes. ±e ascending limb
then uses the increasingly “salty” filtrate leF behind in the de-
scending limb to raise the osmolality of the medullary inter-
stitial fluid even further. ±is establishes a positive feedback
cycle that produces the high osmolality of the fluids in the
descending limb and interstitial fluid.
Notice at the top of the right page of ²igure 25.16 that there
is a constant difference in filtrate concentration (200 mOsm)
between the two limbs of the nephron loop, and between the
ascending limb and the interstitial fluid. ±is difference reflects
the power of the ascending limb’s NaCl pumps, which are just
powerful enough to create a 200 mOsm difference between the
inside and outside of the ascending limb. A 200 mOsm gradi-
ent by itself would not be enough to allow excretion of very
concentrated urine. ±e beauty of this system lies in the fact
that, because of countercurrent flow, the nephron loop is able
to “multiply” these small changes in solute concentration into
a gradient change along the vertical length of the loop (both
inside and outside) that is closer to 900 mOsm (1200 mOsm –
300 mOsm).
Notice also that while much of the Na
and Cl
in the ascending limb is active (via Na
ers in the thick ascending limb), some is passive (mostly in the
thin portion of the ascending limb).
The Countercurrent Exchanger
±e vasa recta act as countercurrent exchangers (²igure
25.16b). Countercurrent exchange does not create the medul-
lary gradient, but preserves it (1) by preventing rapid removal
of salt from the medullary interstitial space, and (2) by remov-
ing reabsorbed water. As a result, blood leaving and reenter-
ing the cortex via the vasa recta has nearly the same solute
±e water picked up by the ascending vasa recta includes not
only water lost from the descending vasa recta, but also water
reabsorbed from the nephron loop and collecting duct. As a
result, the volume of blood at the end of the vasa recta is greater
than at the beginning.
Formation of Dilute or Concentrated Urine
As we have just seen, the kidneys go to a great deal of trouble to
create the medullary osmotic gradient. But for what purpose?
Without this gradient, you would not be able to raise the con-
centration of urine above 300 mOsm—the osmolality of inter-
stitial fluid. As a result, you would not be able to conserve water
when you are dehydrated.
previous page 1010 Human Anatomy and Physiology (9th ed ) 2012 read online next page 1012 Human Anatomy and Physiology (9th ed ) 2012 read online Home Toggle text on/off