Nitric oxide accounts for dose-dependent estrogen mediated coronary relaxation after acute estrogen withdrawal. Circulation 90

Background Estrogen replacement therapy reduces the risk of coronary heart disease in postmenopausal women, and estrogen treatment modulates endothelium-dependent vasodi-lation in ovariectomized, atherosclerotic monkeys. Estradiol-17,3 also induces relaxation in isolated rabbit coronary arteries as well as cerebral basilar arteries. The estrogen concentra-tions required to induce such relaxation are in the pharmaco-logical range (10`6 to 10 ` mol/L). Methods and Results The present study was designed to test whether the sensitivity and specificity of the relaxing response of coronary vascular smooth muscle to exogenous estradiol-17,3 is dependent on the sex hormone status of the animal. In coronary artery rings contracted with PGF2, (3x 10 ` mol/L), estradiol-17, ( caused significant relaxation at a physiological estrogen concentration (10 ` mol/L), in coronary artery rings fro