Endothelium-Derived Endothelin-1 Reduces Cerebral Artery Sensitivity to Nitric Oxide by a Protein Kinase C–Independent Pathway | Zendy

Patricia Gilbert | Zendy; Johanne Tremblay | Zendy; Éric Thorin | Zendy

Open Access

Endothelium-Derived Endothelin-1 Reduces Cerebral Artery Sensitivity to Nitric Oxide by a Protein Kinase C–Independent Pathway

Author(s) -

Patricia Gilbert,

Johanne Tremblay,

Éric Thorin

Publication year - 2001

Publication title -

stroke

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.397

H-Index - 319

eISSN - 1524-4628

pISSN - 0039-2499

DOI - 10.1161/hs1001.096007

Subject(s) - nitric oxide , medicine , sodium nitroprusside , endocrinology , endothelin receptor , vasoconstriction , protein kinase c , endothelin 1 , cerebral arteries , receptor antagonist , vascular smooth muscle , endothelins , acetylcholine , vasodilation , receptor , antagonist , signal transduction , biology , biochemistry , smooth muscle

Nitric oxide (NO) reduces endothelin-1 (ET-1) production and blunts ET-1 dependent vasoconstriction. The direct effects of smooth muscle ET(A) receptor stimulation on NO-mediated relaxation are unknown. We hypothesized that endothelium-derived ET-1 regulates vascular tone by reducing smooth muscle sensitivity to NO, possibly through activation of protein kinase C (PKC).

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