Bradykinin Stimulates Endothelial Nitric Oxide(NO) Production by Calcium/Calmodulin-Dependent NO Synthase.
نویسندگان
چکیده
منابع مشابه
Angiotensin II stimulates synthesis of endothelial nitric oxide synthase.
Previous studies have suggested that NO may play an important role in protecting the renal vessels from angiotensin II (ANGII)-mediated vasoconstriction. One possible mechanism for this interaction is that ANGII could stimulate NO production in the kidney by increasing endothelial NO synthase (NOS III). The present studies were performed in rats to determine whether acute or chronic elevations ...
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Apolipoprotein E (apoE) is widely expressed in mammalian tissues, and one of the important tissue-specific effects is the atheroprotection ascribed to macrophage-derived apoE in the arterial wall. However, underlying mechanisms are not well understood. In this study, using subcellular fractionation, confocal microscopy, and coimmunoprecipitation, we demonstrated that macrophage-derived apoE is ...
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Inducible nitric oxide synthase (iNOS) gene expresses a calcium calmudolin-independent enzyme which can catalyse NO production from L-arginine. The induction of iNOS activity has been demonstrated in a wide variety of cell types under stimulation with cytokines and lipopoly saccharide (LPS). Previous studies indicated that all nitric oxide synthases (NOS) activated in human umbilical vein endot...
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Background: This is a case-control study to determine the relationship between endothelial nitric oxide synthase (eNOS) gene -786T/C polymorphism in women with unexplaiend recurrent abortion in comparison with healty women.Materials and Methods: 95 women with history of at least 2 unexplaiend recurrent abortion in the reproductive age range 20-35 years as patients group and 95 healty women (age...
متن کاملHypercholesterolemia decreases nitric oxide production by promoting the interaction of caveolin and endothelial nitric oxide synthase.
Hypercholesterolemia is a central pathogenic factor of endothelial dysfunction caused in part by an impairment of endothelial nitric oxide (NO) production through mechanisms that remain poorly characterized. The activity of the endothelial isoform of NO synthase (eNOS) was recently shown to be modulated by its reciprocal interactions with the stimulatory Ca2+-calmodulin complex and the inhibito...
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ژورنال
عنوان ژورنال: Hypertension Research
سال: 1993
ISSN: 0916-9636,1348-4214
DOI: 10.1291/hypres.16.131