Abstract
Two female patients with adrenal cortical insufficiency were studied before and after delivery in order to assess the effects of pregnancy upon the sodium-retaining action of administered aldosterone. In both subjects, intravenous administration of large amounts of d-aldosterone (up to 500 μg) exerted negligible effects upon electrolyte excretion before delivery. After delivery the expected sodium-retaining and kaliuretic effects of aldosterone were restored. Although additional explanations are possible, the probable basis for the observed resistance to aldosterone effect during gestation appears to be placental secretion of progesterone, a steroid which has been shown to antagonize aldosterone action.
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