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1 Center for Perinatal BIology, Departments of Physiology/Pharmacology, Loma Linda University, School of Medicine, Loma Linda, CA, USA
2 Center for Perinatal BIology, Departments of Physiology/Pharmacology, Loma Linda University, School of Medicine, Loma Linda, CA, USA; Department of Pediatrics, Loma Linda University, School of Medicine, Loma Linda, CA, USA
* To whom correspondence should be addressed. E-mail: cducsay{at}som.llu.edu.
Exposure to long-term hypoxia (LTH) results in altered cortisol responses in the ovine fetus. The present study was designed to test the hypothesis that LTH alters adrenal responsiveness to fetal hypotension. Pregnant ewes were maintained at high altitude (3,820 m) from day 30 of gestation. Normoxic control and LTH fetuses were catheterized on day 132 of gestation. In the LTH group, maternal PO2 was maintained comparable to that observed at altitude (~60 mmHg) by nitrogen infusion through a tracheal catheter. On day 137, fetuses received a 5 h saline infusion followed by infusion of sodium nitroprusside to reduce fetal arterial pressure by 30-35% for 10 min. The study was repeated on day 139 of gestation with a continuous cortisol infusion (10 µg/min). Hypothalamic and pituitary tissues were collected from additional fetuses for assessment of glucocorticoid receptors. During the saline infusion in response to hypotension, plasma ACTH increased over pre-infusion mean values in both groups (p < 0.05). Plasma cortisol concentrations increased in both groups concomitant with increased ACTH secretion. However, peak values in the LTH fetuses were significantly higher compared with controls (p<0.05). During the cortisol infusion, the ACTH response was eliminated in both groups with ACTH levels significantly lower in the LTH group (p<0.05). Glucocorticoid receptor binding was not different between groups. These results demonstrate an enhanced cortisol response to hypotension in LTH fetuses which does not appear to be the result of an increase in negative feedback sensitivity of the hypothalamic-pituitary-adrenal axis.
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