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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