Physiological inhibition of ovine fetal plasma renin activity by cortisol.
The purpose of this study was to test the hypothesis that physiological increases in the fetal plasma cortisol concentration after basal and stimulated levels of PRA and vasopressin. Seven fetal sheep, between 121 and 131 days gestation, were infused with cortisol (4 micrograms/min) or vehicle for 5 h. One hour after the end of cortisol or vehicle infusion, sodium nitroprusside was infused into the fetus (100 micrograms/min, iv) to stimulate fetal hormone secretion. Cortisol, but not vehicle, infusion increased the fetal plasma cortisol concentration and decreased fetal PRA, but did not alter the fetal plasma vasopressin concentration. Cortisol-infused fetuses responded to nitroprusside with slightly smaller PRA responses but with equal vasopressin responses compared to those of vehicle-infused controls. Fetal blood pressure was not affected by either cortisol or vehicle infusion. Nitroprusside caused a slightly greater reduction in pressure in fetuses receiving cortisol infusion compared to those receiving the vehicle. We conclude that physiological increases in fetal plasma cortisol decrease fetal PRA without altering the fetal plasma vasopressin concentration. The results suggest that repeated fetal stress might produce progressive reduction of fetal PRA activity and might, therefore, alter cardiovascular homeostasis.
D000818:Animals; D001127:Arginine Vasopressin / Q000097:blood; D001794:Blood Pressure / Q000187:drug effects; D005260:Female; D005312:Fetal Blood / Q000032:analysis; D005333:Fetus; D006339:Heart Rate / Q000187:drug effects; D006454:Hemoglobins / Q000032:analysis; D006854:Hydrocortisone / Q000097:blood / Q000494:pharmacology*; D006863:Hydrogen-Ion Concentration; D011247:Pregnancy; D012083:Renin / Q000097:blood*; D012756:Sheep; D000092502:Renin Inhibitors
D001127:Arginine Vasopressin; D006454:Hemoglobins; D006854:Hydrocortisone; D012083:Renin; D000092502:Renin Inhibitors