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Department of Chemistry, California State University, San Bernardino, California 92407
Acute and chronic stresses are implicated
in cardiovascular diseases including coronary artery disease. The
present study was designed to examine the direct effects of the stress
hormone cortisol on nitric oxide (NO) release and endothelial NO
synthase (eNOS) expression in cultured bovine coronary artery
endothelial cells (BCAEC). Nitrate, nitrite, and NO (NOx)
were measured by the chemiluminescence method. At 24 h after
treatment, cortisol (1 nM-10 µM) produced a dose-dependent
decrease in NOx release, which was attenuated in the
presence of the 11
-hydroxysteroid dehydrogenase 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
downregulating 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.
nitric oxide; endothelial nitric oxide synthase; endothelial cell
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