Effects of sex hormones on the renal pressor system.

Abstract

The effects of sex and sex hormones on angiotensinogen, renin activity, and renin concentration in plasma and on renal renin were investigated in rats. During estrus there was a significant increase in angiotensinogen, which was suppressed by ovariectomy. In males, castration had no effect. Administration of stilbestrol caused a rapid increase in angiotensinogen. Renal renin and plasma renin concentration decreased while plasma renin activity remained near normal levels. Following addition of a constant dose of rat renin, plasma from estrogen-treated rats released angiotensin at a faster rate than normal plasma; this increased reactivity is attributed to the high substrate concentration and not to the lack of an inhibitor, to the presence of an activator, or of a more reactive substrate. These changes were not modified by progesterone or testosterone. Progesterone alone caused a significant increase in renal renin. Estrogens did not elicit hypertension nor modify a preexisting renal hypertension. These observations support the hypothesis that the primary effect of estrogens is an increased angiotensinogen formation, and that the resulting enhancement in plasma reactivity to renin causes an increase in angiotensin which acts as a negative feedback on renin production.