作者: M. Dodic , A. T. McAlinden , A. J. Jefferies , E. M. Wintour , M. L. Cock
DOI: 10.1113/JPHYSIOL.2005.102186
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摘要: Prenatal exposure to elevated maternal glucocorticoids (dexamethasone (DEX) or cortisol (CORT)) for 2 days early in pregnancy can 'programme' alterations adult offspring of sheep, including arterial pressure. DEX treatment also results greater angiotensin II type 1 (AT1) receptor expression the medulla oblongata late gestation fetuses than saline (SAL)- CORT-exposed animals. We hypothesized that this would result functional changes brainstem angiotensinergic control cardiovascular function DEX- but not To test hypothesis, responses intracerebroventricular (I.C.V.) were examined male exposed (0.48 mg h(-1); n = 7), CORT (5 h(-1), 6) SAL (n 9) from 26 28 gestation. Increases mean pressure during i.c.v. infusion (1 10 microg h(-1)) significantly group (10 +/- mmHg at compared with (6 mmHg) animals (P < 0.05). I.C.V. AT1 antagonist losartan decreased cardiac output and heart rate animals, Thus, increased mRNA after prenatal is associated responsiveness activation brain AT receptors by exogenous endogenous II. The altered role RAS sheep prenatally was observed cortisol, suggesting these two have distinct programming actions.