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Am J Physiol Heart Circ Physiol 285: H2150-H2157, 2003. First published July 24, 2003; doi:10.1152/ajpheart.00966.2002
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Regulation of nitric oxide-dependent vasodilation in coronary arteries of estrogen receptor-{alpha}-deficient mice

Judy M. Muller-Delp,1 Dennis B. Lubahn,2,3 Kathryn E. Nichol,1 Brian J. Philips,2 Elmer M. Price,4,6 Edward M. Curran,2 and M. Harold Laughlin4,5,6

1Department of Health and Kinesiology, Texas A&M University, College Station, Texas 77843; 2Departments of Biochemistry, 3Child Health, 4Biomedical Sciences, and 5Medical Physiology, 6The Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri 65211

Submitted 7 November 2002 ; accepted in final form 21 July 2003

Estrogen has been shown to increase endothelium-dependent vasodilation and expression of endothelial nitric oxide (NO) synthase (eNOS); however, the role of estrogen receptors in mediating estrogen effects on endothelial function remains to be elucidated. The purpose of this study was to test the hypothesis that estrogen modulates NO-dependent vasodilation of coronary arteries through its action on estrogen receptor-{alpha} (ER-{alpha}) to increase protein levels of eNOS and Cu/Zn superoxide dismutase (SOD-1). Vasodilation to acetylcholine (ACh) and sodium nitroprusside was assessed in isolated coronary arteries from intact and ovariectomized female wild-type (WT) and ER-{alpha} knockout (ER{alpha}KO) mice. Protein levels for eNOS and SOD-1 were also evaluated. Vasodilation to ACh was not significantly altered in ER{alpha}KO mice compared with WT mice. Ovariectomy reduced responsiveness to ACh in ER{alpha}KO mice but not WT mice. Responses to sodium nitroprusside were not altered by disruption of ER-{alpha} or by ovariectomy. Supplementation with estrogen restored ACh-induced vasodilation in ovariectomized ER{alpha}KO mice. eNOS protein was reduced in ER{alpha}KO mice compared with WT mice. Ovariectomy caused a further reduction in eNOS protein in ER{alpha}KO mice, but this reduction was reversed by estrogen treatment. SOD-1 protein levels were increased by disruption of ER-{alpha}. Ovariectomy reduced SOD-1 protein in ER{alpha}KO mice, but this reduction was partially reversed by estrogen replacement. These results suggest that estrogen modulation of eNOS protein content is mediated in part through ER-{alpha}. NO-dependent responses are preserved in ER{alpha}KO mice, possibly through increased SOD-1 expression and enhanced bioavailability of NO.

endothelial nitric oxide synthase; superoxide dismutase; acetylcholine; ovariectomy; sodium nitroprusside


Address for reprint requests and other correspondence: J. M. Muller-Delp, Dept. of Health and Kinesiology, Texas A&M Univ., College Station, TX 77843 (E-mail: jmd{at}hlkn.tamu.edu).




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