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TRPC channel-derived calcium fluxes differentially regulate ATP and flow–induced activation of eNOS

Endothelial dysfunction, characterised by impaired nitric oxide (NO) bioavailability, arises in response to a variety of cardiovascular risk factors and precedes atherosclerosis. NO is produced by tight regulation of endothelial nitric oxide synthase (eNOS) activity in response to vasodilatory stimu...

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Bibliographic Details
Published in:Nitric Oxide
Main Authors: Muzorewa, Tenderano T., Buerk, Donald G., Jaron, Dov, Barbee, Kenneth A.
Format: Artigo
Language:Inglês
Published: 2021
Subjects:
Online Access:https://ncbi.nlm.nih.gov/pmc/articles/PMC8145791/
https://ncbi.nlm.nih.gov/pubmed/33813098
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.niox.2021.03.005
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