Renal function in human pregnancy. III. Effects of antidiuretic hormone (ADH) on renal hemodynamics and water and electrolyte excretion near term and post partum.

Abstract

It has been suggested that pregnant women are less sensitive to the action of ADH because they possess an inactivating mechanism for this hormone. This hypothesis was tested by studying the effects of intravenous administration of Pitressin on renal hemodynamics and water and electrolyte excretion in pregnant women in the latter part of gestation and in postpartum and nonpregnant subjects. During pregnancy, a single intravenous dose of 100 milliunits (m.u.) of Pitressin or continuous infusion of this hormone in doses varying from 25 to 100 m.u. per hour produced a marked fall in urine flow with a simultaneous fall in renal plasma flow, glomerular filtration rate, and the output of sodium, chloride and total solute. Potassium excretion was inconsistent. Osmolal and free water clearances fell, the latter becoming negative in most instances. Following delivery or in the nonpregnant state, the same or higher doses of Pitressin produced a reduction in urine flow which was of the same magnitude and pattern as that in the pregnant subjects. However, renal hemodynamics remained unchanged and electrolyte excretion even increased. This response was typical of the action of Pitressin as described in the literature. Although various hypotheses are offered to explain the altered response to Pitressin in pregnancy, at present it is not possible to identify precisely the factors that account for the change in renal hemodynamics and the fall in solute excretion. The results of the present study do not lend support to the hypothesis suggested by others that an inactivating mechanism for ADH exists in human pregnancy.