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Articles in PresS, published online ahead of print February 28, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00842.2001
Submitted on September 26, 2001
Accepted on February 26, 2002
1 Center for Perinatal Biology, Department of Pharmacology & Physiology, Loma Linda University School of Medicine, Loma Linda, CA, USA
2 Center for Perinatal Biology, Department of Pharmacology & Physiology, Loma Linda University School of Medicine, Loma Linda, CA, USA; Jiangxi Provincial Key Laboratory for Animal Biotechnology, Jiangxi Agricultural University, Nanchang, Jiangxi, China
* To whom correspondence should be addressed. E-mail: lzhang{at}som.llu.edu.
During pregnancy maternal plasma cortisol concentrations approximately double. Given that cortisol plays an important role in the regulation of vascular reactivity, the present study investigated the potential role of cortisol in potentiation of uterine artery (UA) contractility, and tested the hypothesis that pregnancy down-regulated the cortisol-mediated potentiation. In vitro cortisol treatment (3, 10, 30 ng/ml for 24 h) produced a dose-dependent increase in NE-induced contractions in both nonpregnant and pregnant (138 to 143d gestation) sheep UA. However, this cortisol-mediated response was significantly attenuated by ~50% in pregnant UA. The 11ß-hydroxysteroid dehydrogenase (11-ßHSD) inhibitor carbenoxolone did not change cortisol's effect in nonpregnant UA, but abolished its effect in pregnant UA by increasing the NE pD2 in control tissues from 6.20 ± 0.05 to 6.59 ± 0.11. The dissociation constant (KA) value of NE-
1-adrenoceptors was not changed by cortisol in pregnant, but decreased in nonpregnant UA. There was no difference in glucocorticoid receptor density between nonpregnant and pregnant UA. Cortisol significantly decreased eNOS protein levels and NO release in both nonpregnant and pregnant UA, but the cortisol's effect was attenuated in pregnant UA by ~50%. Carbenoxolone alone had no effects on NO release in nonpregnant but decreased it in pregnant UA. The results suggest that cortisol potentiates NE-mediated contractions by decreasing NO release and increasing NE binding affinity to 1-adrenoceptors in nonpregnant uterine artery. Pregnancy attenuates uterine artery sensitivity to cortisol, which may be mediated by increasing type-2 11-ßHSD activity in the uterine artery.
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