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DEFICIENT MICE
1 Department of Health and Kinesiology, Texas A&M University, College Station, Texas, USA
2 Department of Biochemistry, University of Missouri, Columbia, Missouri, USA; Department of Child Health, University of Missouri, Columbia, Missouri, USA
3 Department of Biochemistry, University of Missouri, Columbia, Missouri, USA
4 Department of Biomedical Sciences, University of Missouri, Columbia, Missouri, USA; The Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri, USA
5 Department of Biomedical Sciences, University of Missouri, Columbia, Missouri, USA; Department of Medical Physiology, University of Missouri, Columbia, Missouri, USA; The Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri, USA
* To whom correspondence should be addressed. E-mail: jmd{at}hlkn.tamu.edu.
Estrogen has been shown to increase endothelium-dependent vasodilation and expression of endothelial nitric oxide synthase (ecNOS); 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 nitric oxide-dependent vasodilation of coronary arteries through its action on estrogen receptor 
(ER-) to increase protein levels of ecNOS and Cu/Zn superoxide dismutase (SOD-1). Vasodilation to acetylcholine and sodium nitroprusside was assessed in isolated coronary arteries from intact and ovariectomized female wild-type (WT) and estrogen receptor knockout (ERKO) mice. Protein levels for ecNOS and SOD-1 were also evaluated. Vasodilation to acetylcholine was not significantly altered in ERKO mice as compared to WT mice. Ovariectomy reduced responsiveness to acetylcholine in ERKO mice but not WT mice. Responses to sodium nitroprusside were not altered by disruption of ER- or by ovariectomy. Supplementation with estrogen restored ACh-induced vasodilation in ovariectomized ERKO mice. ecNOS protein was reduced in ERKO mice compared to WT mice. Ovariectomy caused a further reduction in ecNOS protein in ERKO mice, but this reduction was reversed by estrogen treatment. SOD-1 protein levels were increased by disruption of ER-. Ovariectomy reduced SOD-1 protein in ERKO mice, but this reduction was reversed by estrogen replacement. These results suggest that estrogen modulation of ecNOS protein content is mediated in part through ER-. Nitric oxide-dependent responses are preserved in ERKO mice, possibly through increased expression SOD-1 and enhanced bioavailability of nitric oxide.
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