(Hypertension. 1996;28:330-334.)
© 1996 American Heart Association, Inc.
Articles |
the Alfred & Baker Medical Unit and Menopause Clinic, Baker Medical Research Institute and Alfred Hospital, Melbourne, Australia.
Correspondence to Dr K. Sudhir, Box 0124, University of California, 505 Parnassus Ave, San Francisco, CA 94143-0124. E-mail sudhir@cardio.ucsf.edu.
The mechanisms of estrogen-induced cardiovascular protection are incompletely understood. Acute estrogen administration enhances acetylcholine-induced vasorelaxation, suggesting that endothelium-dependent factors may be important. The effect of long-term estrogen supplementation on endothelial function has not been well defined. In this double-blind, randomized study, we examined endothelial function in forearm resistance arteries in 11 perimenopausal women before and after 8 weeks of estrogen supplementation (estradiol valerate, 2 mg daily, n=6) or placebo (n=5). Forearm blood flow was measured by venous-occlusion plethysmography, and vasoactive agents were infused through a brachial artery cannula in doses that did not influence blood pressure or heart rate. Estrogen supplementation significantly reduced systolic and diastolic pressures but had no effect on plasma lipoproteins. Estrogen did not alter the vasodilator responses to acetylcholine at doses of 9.25, 18.5, and 37 µg/min (rise in forearm blood flow before estrogen: 263±72%, 288±66%, and 383±84%, respectively; after estrogen: 205±34%, 260±44%, and 359±54%, P>.05.). Vasodilator responses to the endothelium-independent agent sodium nitroprusside (1.6 µg/min) were also unchanged after estrogen supplementation. However, estrogen enhanced vasoconstrictor responses to the nitric oxide synthase inhibitor NG-monomethyl-L-arginine at doses of 1, 2, and 4 µmol/min (fall in forearm blood flow before estrogen: 13±9%, 20±7%, and 26±8%, respectively; after estrogen: 18±9%, 36±7%, and 47±7%, P=.04). Responses to vasoactive agents were unchanged after administration of placebo. Thus, in perimenopausal women, estrogen supplementation reduces blood pressure and enhances basal but not acetylcholine-induced nitric oxide release in forearm resistance arteries.
Key Words: estrogens nitric oxide menopause plethysmography endothelium, vascular
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