Abstract
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 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.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adrenergic alpha-Agonists / pharmacology
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Animals
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Aorta
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Blood Pressure
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Cells, Cultured
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Estradiol / analogs & derivatives*
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Estradiol / pharmacology
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Estrogen Antagonists / pharmacology
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Estrogen Receptor alpha
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Estrogen Receptor beta
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Fulvestrant
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Guanidines / pharmacology
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Humans
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Hypertension / physiopathology*
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In Vitro Techniques
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Male
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Mice
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Mice, Knockout
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Muscle, Smooth, Vascular / physiology*
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Nitric Oxide Synthase / genetics
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Nitric Oxide Synthase / metabolism
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Nitric Oxide Synthase Type II
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Nitroarginine / pharmacology
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Patch-Clamp Techniques
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Phenylephrine / pharmacology
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Potassium Channels / metabolism
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Receptors, Estrogen / genetics
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Receptors, Estrogen / physiology*
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Vasoconstriction* / drug effects
Substances
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Adrenergic alpha-Agonists
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Estrogen Antagonists
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Estrogen Receptor alpha
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Estrogen Receptor beta
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Guanidines
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Potassium Channels
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Receptors, Estrogen
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Phenylephrine
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Nitroarginine
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Fulvestrant
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Estradiol
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NOS2 protein, human
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Nitric Oxide Synthase
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Nitric Oxide Synthase Type II
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Nos2 protein, mouse
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pimagedine