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Ovariectomy impairs estrogen‐induced relaxation of mesenteric microvessels
Author(s) -
Royal Crista Ruth,
White Richard E
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.742.6
Subject(s) - estrogen , endocrinology , mesenteric arteries , medicine , endothelium , nitric oxide , vasodilation , blood vessel , menopause , coronary arteries , chemistry , artery
The effect of estrogen on the cardiovascular health of postmenopausal women has become highly controversial, particularly in light of recent clinical trials such as the Women's Health Initiative. Prior to such trials estrogen was believed to be primarily cardio‐protective, an effect at least partially due to its ability to relax blood vessels. We had demonstrated that 17β‐estradiol (E 2 ) relaxed porcine coronary arteries by an endothelium‐independent mechanism involving stimulation of neuronal nitric oxide synthase (nNOS) in smooth muscle cells. We now report that artificially inducing menopause by ovariectomy (OVX) almost completely abolishes E 2 –induced, endothelium‐independent relaxation of rat mesenteric arteries. In contrast, estrogen relaxed mesenteric microvessels from OVX rats in the presence of an intact endothelium. Inhibition of NOS activity with either 0.1mM L‐NAME or 1mM L‐NMMA abolished this relaxant effect of E2 in intact vessels from an OVX rat. Our results indicate endothelium‐independent, estrogen‐induced relaxation of resistance arteries is attenuated in postmenopausal rats compared to age‐matched control animals. (supported by HL073890)