ANGIOTENSIN-II INFUSION IN-VIVO DOES NOT MODULATE CORTISOL SECRETION IN THE LATE-GESTATION OVINE FETUS

Maturation of the fetal adrenal gland is critical for the onset of ovi ne parturition. It has long been proposed that the fetal adrenal gland may be under inhibitory influences during late gestation. In vitro ev idence has suggested that angiotensin II may be such an inhibitory fac tor and may help to prevent a premature increase in cortisol concentra tions. The aim of this study was to test the effect of angiotensin II infusion in vivo on basal cortisol concentrations and fetal adrenal re sponsiveness to an ACTH-(1-24) challenge. Fetuses received a continuou s infusion of either angiotensin II (100 ng.min(-1).kg(-1); n = 7) or saline (2 ml/h; n = 4), which commenced at 140 days of gestation (GA) and continued for a total of 50 h. Adrenal responsiveness to the admin istration of ACTH-(1-24) (5 mu g/kg) was determined during angiotensin II or saline infusions at both 2 and 48 h after infusion onset. Angio tensin II had no significant effect on adrenal responsiveness after ac ute (2 h) or chronic (48 h) infusion. There was no effect of saline or angiotensin II infusion on basal immunoreactive ACTH or cortisol conc entrations after 2 h, but there was a significant increase in basal co rtisol concentrations in both treatment groups by 48 h, probably refle cting the normal rise in cortisol concentrations at this GA. Mean arte rial blood pressure was significantly increased in angiotensin II-infu sed fetuses only. This study has therefore found no evidence to sugges t that angiotensin II infusion in vivo modulates fetal basal cortisol concentrations or adrenal responsiveness in the last week of gestation , in contrast with previous in vitro studies. These results throw into question the proposed role of angiotensin II as a negative modulator of adrenal function in the ovine fetus.