Baroreceptor and prostanoid control of fetal renal cortical blood flow and plasma renin activity

Abstract

Renal function in the fetus is important for maintenance of fetal fluid and electrolyte balance. This study was performed to test the role of prostaglandins and their interaction with arterial baroreceptors and chemoreceptors in the control of renal cortical blood flow during hypotension produced by vena caval obstruction in late-gestation fetal sheep. We studied 18 time-dated, chronically catheterized, fetal sheep (124–136 days gestation). Fetuses were either studied intact (n = 11) or sinoaortic denervated (n = 7), and each fetus was studied twice, with and without pretreatment with indomethacin (0.2 mg kg ^–1 , i.v.). Each fetus was subjected to hypotension caused by vena caval obstruction for 10 min. Before hypotension, renal cortical blood flow was higher in the vehicle-treated sinoaortic denervated fetuses than in vehicle-treated intact fetuses. The increased renal cortical blood flow observed in the sinoaortic denervated fetuses was counteracted by indomethacin, so that the difference between sinoaortic denervated and intact fetuses was eliminated after indomethacin treatment. Hypotension decreased renal blood flow equally in all groups. Plasma renin activity was increased in response to hypotension in the intact fetuses, but not in the sinoaortic denervated fetuses. Indomethacin treatment, by itself, did not alter plasma renin activity. It is concluded that both arterial baroreceptors and prostanoids influence renal blood flow. Further, renin secretion is influenced by arterial baroreceptors and chemoreceptors and there is no apparent modulatory effect of prostanoids on the baroreflex control of renin secretion.