Estrogen Modulation of Endothelial Nitric Oxide Synthase
نویسندگان
چکیده
منابع مشابه
Endothelial nitric oxide synthase and estrogen.
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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The endothelial NO synthase (eNOS) is regulated by diverse protein kinase pathways, yet eNOS activity ultimately depends on the ubiquitous calcium regulatory protein calmodulin (CaM). In these studies, we establish that CaM itself undergoes phosphorylation in endothelial cells and that CaM phosphorylation attenuates eNOS activation. Using [(32)P]orthophosphoric acid biosynthetic labeling, we fo...
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متن کاملEstrogen 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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ژورنال
عنوان ژورنال: Endocrine Reviews
سال: 2002
ISSN: 0163-769X,1945-7189
DOI: 10.1210/er.2001-0045