Role of angiotensin II on the adrenal and vascular responses to hemorrhage during development in fetal lambs.

Abstract

Developmental aspects of fetal adrenal and vascular responses to endogenous increase in plasma angiotensin II (AII) following sequential reductions of fetoplacental blood volume were studied in 2 groups of chronically catheterized fetal lambs (7 were < 120 days and 7 were > 130 days of gestation, term being 145 days). At similar levels of hemorrhage, the rise in plasma renin activity (PRA) was greater in fetuses > 130 days than in those < 120 days (P < 0.025). The effect of hemorrhage on plasma AII was also more pronounced in fetuses > 130 days (P < 0.05). No changes in plasma aldosterone were seen during hemorrhage in fetuses < 120 days; plasma aldosterone increased (P < 0.001) in those > 130 days. This increase correlated with the rise in plasma AII (r = 0.70, P < 0.001). To determine whether factors other than the rise in plasma AII were responsible for the increase in plasma aldosterone in fetuses > 130 days, these results were compared to results obtained in 4 nephrectomized fetuses > 130 days submitted to similar degrees of hemorrhage. No changes in PRA or plasma AII were observed. A small increase in plasma aldosterone (from 31 .+-. 13 to 47 .+-. 11 pg/ml, P < 0.01) was found, and this correlated with changes in plasma K concentration (r = 0.50, P < 0.05). Mean arterial blood pressure decreased during hemorrhage in fetuses < 120 days (P < 0.05); no changes were observed in those > 130 days unless their kidneys were removed. Apparently, renin-angiotensin system is an important modulator of fetal blood pressure during hemorrhagic stress.