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First published online on January 17, 2003.
 Copyright © 2003 by The Physiological Society
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2002.032565v1
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Received September 14, 2002
Accepted after revision January 9, 2003

Prenatal dexamethasone leads to both endothelial dysfunction and vasodilatory compensation in sheep

Judit Molnar1, David C. Howe1, Mark J.M. Nijland1, and P. W. Nathanielsz2*

1 Edward Melby Cardiovascular Research Laboratory, Laboratory for Pregnancy and Newborn Research, Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York, 14850 USA
2 LPNR Box 16, Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York 14853, USA

* To whom correspondence should be addressed. E-mail: pwn1{at}cornell.edu.

We investigated long-term cardiovascular effects in the offspring of sheep exposed to prenatal dexamethasone (DM). We assessed in vitro vascular responsiveness and evaluated endothelial nitric oxide synthase (eNOS) message and protein levels in femoral muscle removed from 5-month-old sheep. Dexamethasone was administered i.m. to pregnant ewes as 3 weekly courses (4 x 2 mg at 12 h intervals), starting on day 103 gestation (term ~149 days). Ewes were allowed to lamb. At 5 months of age a carotid catheter was placed for blood pressure measurement and hamstring muscle was removed from the lambs under general anaesthesia. We demonstrate that following prenatal DM exposure in the 5-month-old offspring: (1) blood pressure is unchanged; (2) as previously reported in the fetus, sensitivity to endothelin-1 (ET) is increased; (3) acetylcholine-induced relaxation is increased; (4) L-NAME suppressible vasodilatory response to ET is abolished; (5) no change in endothelium-independent vasodilatation; and (6) no change in eNOS RNA and protein levels, when compared to saline treated controls. We speculate that decreased agonist-induced NO release is not due to alteration in gene expression, but it is more likely to be a post-transcriptional event. In summary, the lack of a difference in resting mean arterial pressure (MAP) between DM and control lambs indicates that the compensation we have previously demonstrated in the fetus following glucocorticoid exposure persists to 5 months postnatal age. Compensation is likely due to non NO-dependent mechanisms, since no evidence was found of upregulated NOS.




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