Endogenous prostanoids modulate the ACTH and AVP responses to hypotension in late-gestation fetal sheep

Abstract

We have previously reported that prostaglandin E2 and thromboxane A2 stimulate endocrine and cardiovascular responses similar to the responses to arterial hypotension. The present experiments were designed to test the hypothesis that prostanoids are involved in the generation of responses to hypotension induced by vena cava occlusion. Fetal sheep were either intact or subjected to a prior carotid sinus denervation and bilateral vagosympathetic nerve section. Indomethacin or vehicle was injected intravenously 90 min before the start of arterial hypotension. In intact fetuses treated with phosphate buffer, ACTH increased significantly from 83 ± 39 to 3,611 ± 774 pg/ml, arginine vasopressin (AVP) increased from 3.9 ± 0.5 to 1,079 ± 549 pg/ml, and cortisol increased from 4.7 ± 0.8 to 9.5 ± 1.7 ng/ml. Indomethacin treatment significantly reduced the magnitudes of the hormonal responses. Baroreceptor and chemoreceptor denervation attenuated the ACTH and AVP responses, but these responses were not further inhibited by indomethacin. We conclude that endogenous prostanoids partially mediate the reflex hormonal and hemodynamic responses to arterial hypotension in late-gestation fetal sheep.