Journal
SCIENCE
Volume 295, Issue 5554, Pages 505-508Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1065250
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Funding
- NHLBI NIH HHS [R01 HL56069, HL53546, HL56235, P50 HL63494, R01 HL61298, R01 HL55309] Funding Source: Medline
- NICHD NIH HHS [HD30276] Funding Source: Medline
- NIGMS NIH HHS [GM20069] Funding Source: Medline
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Blood vessels express estrogen receptors, but their rote in cardiovascular physiology is not wet[ understood. We show that vascular smooth muscle cells and blood vessels from estrogen receptor beta (ERbeta)-deficient mice exhibit multiple functional abnormalities. In wild-type mouse blood vessels, estrogen attenuates vasoconstriction by an ERbeta-mediated increase in inducible nitric oxide synthase expression. In contrast, estrogen augments vasoconstriction in blood vessels from ERbeta-deficient mice. Vascular smooth muscle cells isolated from ERbeta-deficient mice show multiple abnormalities of ion channel function. Furthermore, ERbeta-deficient mice develop sustained systolic and diastolic hypertension as they age. These data support an essential role for ERbeta in the regulation of vascular function and blood pressure.
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