Estrogen receptor α mediates the nongenomic activation of endothelial nitric oxide synthase by estrogen
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منابع مشابه
Estrogen receptor alpha mediates the nongenomic activation of endothelial nitric oxide synthase by estrogen.
Estrogen is an important vasoprotective molecule that causes the rapid dilation of blood vessels by activating endothelial nitric oxide synthase (eNOS) through an unknown mechanism. In studies of intact ovine endothelial cells, 17beta-estradiol (E2) caused acute (five-minute) activation of eNOS that was unaffected by actinomycin D but was fully inhibited by concomitant acute treatment with spec...
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BACKGROUND Nontranscriptional signaling through estrogen receptors (ERs) is important in the cardiovascular system. In particular, estrogen stimulates endothelial NO synthase (eNOS) via the phosphatidylinositol 3-kinase (PI3K) pathway. The selective estrogen receptor modulator (SERM) raloxifene is effective for the treatment of postmenopausal osteoporosis, but its ability to activate eNOS via P...
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See article by M.R. Andersen and S. Stender [1] (pages arginine to L-citrulline and nitric oxide (NO). Since NO 192 –199) in this issue. and citrulline are formed in equi-molar quantities, NO formation was expressed in terms of citrulline production Andersen and Stender [1] have reported regional variaper million endothelial cells. Thus it was possible to tions in endothelial nitric oxide synth...
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17b-Estradiol (E2) is a rapid activator of endothelial nitric oxide synthase (eNOS). The product of this activation event, NO, is a fundamental determinant of cardiovascular homeostasis. We previously demonstrated that E2-stimulated endothelial NO release can occur without an increase in cytosolic Ca. Here we demonstrate for the first time, to our knowledge, that E2 rapidly induces phosphorylat...
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ژورنال
عنوان ژورنال: Journal of Clinical Investigation
سال: 1999
ISSN: 0021-9738
DOI: 10.1172/jci5347