Abnormal vascular function and hypertension in mice deficient in estrogen receptor β

Y Zhu, Z Bian, P Lu, RH Karas, L Bao, D Cox, J Hodgin… - Science, 2002 - science.org
Y Zhu, Z Bian, P Lu, RH Karas, L Bao, D Cox, J Hodgin, PW Shaul, P Thorén, O Smithies…
Science, 2002science.org
Blood vessels express estrogen receptors, but their role in cardiovascular physiology is not
well understood. We show that vascular smooth muscle cells and blood vessels from
estrogen receptor β (ERβ)–deficient mice exhibit multiple functional abnormalities. In wild-
type mouse blood vessels, estrogen attenuates vasoconstriction by an ERβ-mediated
increase in inducible nitric oxide synthase expression. In contrast, estrogen augments
vasoconstriction in blood vessels from ERβ-deficient mice. Vascular smooth muscle cells …
Blood vessels express estrogen receptors, but their role in cardiovascular physiology is not well understood. We show that vascular smooth muscle cells and blood vessels from estrogen receptor β (ERβ)–deficient mice exhibit multiple functional abnormalities. In wild-type mouse blood vessels, estrogen attenuates vasoconstriction by an ERβ-mediated increase in inducible nitric oxide synthase expression. In contrast, estrogen augments vasoconstriction in blood vessels from ERβ-deficient mice. Vascular smooth muscle cells isolated from ERβ-deficient mice show multiple abnormalities of ion channel function. Furthermore, ERβ-deficient mice develop sustained systolic and diastolic hypertension as they age. These data support an essential role for ERβ in the regulation of vascular function and blood pressure.
AAAS