Background: At physiological concentrations, 17β-estradiol selectively enhances endothelium-dependent coronary vasodilation by an unknown mechanism in postmenopausal women. Methods and Results: To assess the contribution of nitric oxide (NO) to the vascular effects of estradiol, we measured coronary epicardial and microvascular responses to intracoronary acetylcholine (range, 3 to 300 μg/min for 2 minutes) before and after intracoronary estradiol 75 ng/min for 15 minutes in 20 estrogen-deficient women, 16 of whom had angiographic evidence of atherosclerosis or risk factors for atherosclerosis. This testing was repeated after inhibition of NO synthesis with intracoronary N(G)-monomethyl-L-arginine (L-NMMA) 64 μmol/min for 5 minutes. Estradiol increased acetylcholine-stimulated coronary flow from 54±48% (mean±SD) above baseline values before estradiol infusion to 100±63% above baseline values (P=.007) and decreased coronary resistance from 32±21% to 46±15% below baseline values (P=.007) at a coronary sinus estradiol concentration of 1725±705 pmol/L (470±192 pg/mL). Estradiol also tended to lessen the severity of acetylcholine-induced epicardial coronary artery vasoconstriction from 8±11% to 3±11% below baseline values (P=.123). However, during L-NMMA infusion, estradiol no longer potentiated the effects of acetylcholine on coronary flow dynamics; coronary flow increased 39±46% above baseline values and coronary resistance decreased 19±30% below baseline values (both P<.001 versus pre-L-NMMA responses). The epicardial diameter decreased 8±11% below baseline values (P=.06 versus pre-L-NMMA response). Conclusions: The effects of estradiol at physiological concentrations on endothelium-dependent coronary vasodilator responsiveness in postmenopausal women are mediated by enhanced bioavailability of NO, which may be responsible in part for the cardioprotective effects of estrogen.
|Number of pages||7|
|State||Published - 4 Nov 1997|
- Coronary disease
- Nitric oxide