Inhibition of acth secretion blocks the hypoxia-induced increase of
adrenal cortical blood flow in fetal sheep.
Carter, Anthony M., Jacobus Homan, Mhoyra Fraser, Bryan S. Richardson,
and John R. G. Challis.
Departments of Obstetrics and Gynaecology and Physiology, Lawson
Research Institute, University of Western Ontario, London, Ontario
N6A 4V2, Canada; and Department of Physiology, University of Odense,
DK-5000 Odense, Denmark
APStracts 2:0091E, 1995.
To examine the role of endogenous ACTH in adrenal blood flow responses
to hypoxia, we studied unanesthetized ovine fetuses during an
intravenous infusion of cortisol or vehicle. Fetal hypoxia was
induced after 5h of cortisol or vehicle infusion. Control fetuses
were not made hypoxic. Blood flows were determined before and at 3
time points during the infusions. At 2h and 6h of hypoxia, in
vehicle-infused fetuses, fetal plasma concentrations of IR-ACTH had
risen from 9+/-3 pg/mL to 68+/-25 and 127+/-37 pg/mL, respectively
(mean+/-SE). No significant change in fetal plasma IR-ACTH occurred
in the other groups. Adrenal cortical blood flow rose 3- to 4-fold
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 the control
groups. Thus, prior infusion of cortisol suppressed the rise in fetal
plasma ACTH during hypoxia and selectively blocked the increase in
adrenal cortical blood flow.
Received 23 February 1995; accepted in final form 19 April 1995.
APS Manuscript Number E82-5.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 2 May 1995.