STUDIES ON TOXEMIA OF PREGNANCY: EFFECT OF DESOXYCORTICOSTERONE ACETATE (DCA) ON HEMODYNAMICS AND ELECTROLYTE BALANCE OF NORMAL PREGNANT WOMEN*

Abstract

THE role of desoxycorticosterone acetate (DCA) in the genesis of hypertension has received considerable attention. DCA may produce hypertension by its effect on electrolyte metabolism or by an action on the kidney (1). The symptoms of edema, hypertension and proteinuria characteristic of toxemia of pregnancy are similar in some respects to those observed in DCA overdosage in animals (2–5). This similarity has led to the hypothesis that toxemia of pregnancy may be caused by excessive secretion of DCA or DCA-like substances by the placenta or the adrenals (2–5). That the elevated blood pressure of toxemia of pregnancy may be humoral in origin is suggested by Dexter's observation (6) that renin is present in the blood. Also, ganglionic blockade with tetraethylammonium chloride (TEAC) in patients with toxemia does not produce the pronounced drop in blood pressure observed in normotensive pregnant women (7, 8, 9). This fact augments the evidence suggesting the presence of a humoral agent in toxemia and provides helpful means for evaluating early changes in the direction of toxemia. The present study was undertaken in order to determine if the shortterm administration of DCA to normotensive pregnant women, would reproduce any of the physiologic changes observed in toxemia of pregnancy.