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

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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.