Role of ADH in Controlling Renal
Water Excretion
As discussed, ADH plays an important role in allowing the kidneys
to form a small volume of concentrated urine while excreting normal amounts of
salt. This effect is especially important during water deprivation, which
strongly elevates plasma levels of ADH that in turn increase water reabsorption
by the kidneys and help to minimize the decreases in extra-cellular fluid
volume and arterial pressure that would otherwise occur. Water deprivation for
24 to 48 hours normally causes only a small decrease in extracellular fluid
volume and arterial pressure. However, if the effects of ADH are blocked with a
drug that antago-nizes the action of ADH to promote water reabsorp-tion in the
distal and collecting tubules, the same period of water deprivation causes a
substantial fall in both extracellular fluid volume and arterial pressure.
Conversely, when there is excess extracellular volume, decreased ADH levels reduce reabsorption
of water bythe kidneys, thus helping to rid the body of the excess volume.
Excess ADH Secretion Usually Causes Only Small
Increases in Extracellular Fluid Volume but Large Decreases in Sodium Con- centration. Although ADH is important in
regulatingextracellular fluid volume, excessive levels of ADH seldom cause
large increases in arterial pressure or extracellular fluid volume. Infusion of
large amounts of ADH into animals initially causes renal retention of water and
a 10 to 15 per cent increase in extracellular fluid volume. As the arterial
pressure rises in response to this increased volume, much of the excess volume
is excreted because of the pressure diuresis mecha-nism. After several days of
ADH infusion, the blood volume and extracellular fluid volume are elevated no
more than 5 to 10 per cent, and the arterial pressure is also elevated by less
than 10 mm Hg. The same is true for patients with inappropriate ADH syndrome, in which ADH levels may be elevated
severalfold.
Thus, high levels of ADH do not cause major increases of either
body fluid volume or arterial pres-sure, although high ADH levels can cause severe reduc-tions in extracellular sodium
ion concentration. Thereason for this is that increased water reabsorption
by the kidneys dilutes the extracellular sodium, and at the same time, the
small increase in blood pressure that does occur causes loss of sodium from the
extracellu-lar fluid in the urine through pressure natriuresis.
In patients who have lost their ability to secrete ADH because of
destruction of the supraoptic nuclei, the urine volume may become 5 to 10 times
normal. This is almost always compensated for by ingestion of enough water to
maintain fluid balance. If free access to water is prevented, the inability to
secrete ADH may lead to marked reductions in blood volume and arterial
pressure.
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