ENDOGENOUS ESTROGEN AND ACETYLCHOLINE-INDUCED VASODILATION IN NORMOTENSIVE WOMEN

Acute exogenous estrogen administration en hances endothelial function in postmenopausal women. To evaluate the effect of endogenous estroge n on endothelium-dependent vasodilation, in 10 fertile normotensive wo men (age range 45 to 51 years) we studied the changes in forearm blood flow (strain-gauge plethysmography) induced by intrabrachial acetylch oline (0.15, 0.45, 1.5, 4.5, 15 mu g . 100 mL(-1) . min(-1)), an endot helium-dependent vasodilator, or sodium nitroprusside (1, 2, 4 mu g . 100 mL(-1) . min(-1)), an endothelium-independent vasodilator, in basa l conditions and within 1 month after ovariectomy. As control subjects , 10 matched healthy women were also evaluated. In basal condition, va sodilation to acetylcholine and sodium nitroprusside was similar in pa tients and control subjects. Ovariectomy was followed by endogenous es trogen deprivation (from 71.6+/-31.3 to <12 pg/mL) and was associated with a significant (P<.01) reduction in acetylcholine-induced vasodila tion compared with baseline (maximum percent increase in forearm blood flow: baseline 568.2+/-47.1%; ovariectomy 309.5+/-37.4%); the respons e to sodium nitroprusside was unaffected by ovariectomy (maximum perce nt increase in forearm blood flow: baseline 526.4+/-36.5%; ovariectomy 454.7+/- 47.2%; P=NS). In 6 of 10 patients, the study was repeated af ter 3 months of estrogen replacement therapy (17 beta-estradiol, 50 mu g/d by transdermal patches). Exogenous estrogen restored acetylcholin e-induced vasodilation (maximum percent increase in forearm blood flow : 548.9+/-43.1%; P<.01 versus ovariectomy), which was no longer differ ent from baseline, whereas the response to sodium nitroprusside was no t affected (maximum percent increase in forearm blood flow: 480.2+/-39 .3%; P=NS). These results suggest a protective role of endogenous estr ogen on endothelium-dependent vasodilation in the forearm vascular bed of normotensive women.