ArticleJournal of vascular research2013
Coordinated endothelial nitric oxide synthase activation by translocation and phosphorylation determines flow-induced nitric oxide production in resistance vessels.
Article in Journal of vascular research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Role of L-Arginine and Tetrahydrobiopterin in Attenuation of Vascular Ang1-8 Reactivity via Endothelial PI3K/AKT/eNOS Signaling Pathways in HgCl2-Induced Vascular Dysfunction. An Ex-Vivo Study.Cardiovascular toxicology · 2026Article
- Subcellular Localization Guides eNOS Function.International journal of molecular sciences · 2024Review
- Red blood cells in type 1 diabetes and multiple sclerosis and technologies to measure their emerging roles.Journal of translational autoimmunity · 2022Review
- Caveolae and lipid sorting: Shaping the cellular response to stress.The Journal of cell biology · 2020Review
- Endothelial nitric oxide synthase activation is required for heparin receptor effects on vascular smooth muscle cells.American journal of physiology. Cell physiology · 2020Article
- CGRP signalling inhibits NO production through pannexin-1 channel activation in endothelial cells.Scientific reports · 2019Article
- Evidence of sex differences in the acute impact of oscillatory shear stress on endothelial function.Journal of applied physiology (Bethesda, Md. : 1985) · 2019Article
- Pro-atherosclerotic disturbed flow disrupts caveolin-1 expression, localization, and function via glycocalyx degradation.Journal of translational medicine · 2018Article
- Flow does not alter eNOS phosphoryation at Ser1179 or Thr495 in preconstricted mouse mesenteric arteries.Physiological reports · 2018Article
- Flow-mediated dilation stimulated by sustained increases in shear stress: a useful tool for assessing endothelial function in humans?American journal of physiology. Heart and circulatory physiology · 2018Review
- Article
- Exercise training improves vascular mitochondrial function.American journal of physiology. Heart and circulatory physiology · 2016Article
- Caveolin-1 in Cardiovascular Disease: A Double-Edged Sword.Diabetes · 2015Article
- Loss of function in heparan sulfate elongation genes EXT1 and EXT 2 results in improved nitric oxide bioavailability and endothelial function.Journal of the American Heart Association · 2014Article
- Vascular hypercontractility and endothelial dysfunction before development of atherosclerosis in moderate dyslipidemia: role for nitric oxide and interleukin-6.American journal of cardiovascular disease · 2014Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
BACKGROUND/
aimsEndothelial nitric oxide synthase (eNOS) is associated with caveolin-1 (Cav-1) in plasma membrane. We tested the hypothesis that eNOS activation by shear stress in resistance vessels depends on synchronized phosphorylation, dissociation from Cav-1 and translocation of the membrane-bound enzyme to Golgi and cytosol.
methodsIn isolated, perfused rat arterial mesenteric beds, we evaluated the effect of changes in flow rate (2-10 ml/min) on nitric oxide (NO) production, eNOS phosphorylation at serine 1177, eNOS subcellular distribution and co-immunoprecipitation with Cav-1, in the presence or absence of extracellular Ca(2+).
resultsIncreases in flow induced a biphasic rise in NO production: a rapid transient phase (3-5-min) that peaked during the first 15 s, followed by a sustained phase, which lasted until the end of stimulation. Concomitantly, flow caused a rapid translocation of eNOS from the microsomal compartment to the cytosol and Golgi, paralleled by an increase in eNOS phosphorylation and a reduction in eNOS-Cav-1 association. Transient NO production, eNOS translocation and dissociation from Cav-1 depended on extracellular Ca(2+), while sustained NO production was abolished by the PI3K-Akt blocker wortmannin.
conclusionsIn intact resistance vessels, changes in flow induce NO production by transient Ca(2+)-dependent eNOS translocation from membrane to intracellular compartments and sustained Ca(2+)-independent PI3K-Akt-mediated phosphorylation.
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