INHIBITION OF ACTH-SECRETION BLOCKS HYPOXIA-INDUCED INCREASE OF ADRENAL-CORTICAL BLOOD-FLOW IN FETAL SHEEP

To examine the role of endogenous adrenocorticotropic hormone (ACTH) i n adrenal blood flow responses to hypoxia, we studied unanesthetized o vine fetuses during an intravenous infusion of cortisol or vehicle. Fe tal hypoxia was induced after 5 h of cortisol or vehicle infusion. Con trol fetuses were not made hypoxic. Blood flows were determined before and at three time points during the infusions. At 2 and 6 h of hypoxi a, in vehicle-infused fetuses, fetal plasma concentrations of immunore active ACTH (irACTH) had risen from 9 +/- 3 (SE) pg/ml to 68 +/- 25 an d 127 +/- 37 pg/ml, respectively. No significant change in fetal plasm a irACTH occurred in the other groups. Adrenal cortical blood flow ros e three- to fourfold during hypoxia in vehicle-infused fetuses but did not change from prehypoxia levels in cortisol-infused fetuses (P < 0. 005). Medullary flow rose with hypoxemia, and this was not affected by concurrent cortisol infusion. Adrenal blood flows did not change in t he control groups. Thus prior infusion of cortisol suppressed the rise in fetal plasma ACTH during hypoxia and selectively blocked the incre ase in adrenal cortical blood flow.