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Articles in PresS, published online ahead of print June 27, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00364.2002
Submitted on April 29, 2002
Accepted on June 26, 2002
1 Chemistry, California State University San Bernardino, San Bernardino, CA, USA
* To whom correspondence should be addressed. E-mail: syang{at}csusb.edu.
Acute and chronic stresses are implicated in cardiovascular diseases including coronary artery disease. The present study was designed to examine the direct effects of stress hormone cortisol on nitric oxide release and endothelial nitric oxide synthase (eNOS) expression in cultured bovine coronary artery endothelial cells (BCAEC). NOx (nitrate, nitrite, and nitric oxide) was measured by chemiluminescence method. At 24 h treatment, cortisol (1 nM to 10 µM) produced a dose-dependent decrease in NOx release, which was attenuated in the presence of the 11ß-hydroxysteroid dehydrogenase (11ß-HSD) inhibitor carbenoxolone (3 µM). In accordance, eNOS protein levels were significantly decreased by cortisol in a dose-dependent manner. Cortisol pretreatment significantly increased the rate of eNOS protein degradation in the presence of cycloheximide. In addition, cortisol pretreatment decreased ATP-induced intracellular Ca2+ elevation and NOx release in BCAEC. The presence of glucocorticoid receptors in BCAEC was demonstrated by Western blot. The results suggest that cortisol, through activation of glucocorticoid receptors, suppresses NOx release in BCAEC by down-regulating eNOS proteins and inhibiting intracellular Ca2+ mobilization. Decreased NOx is likely to result in an increase in contraction of coronary arteries, leading to a decrease in coronary blood flow.
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