Bradykinin-Induced Dilation of Human Coronary Arterioles Requires NADPH Oxidase–Derived Reactive Oxygen Species | Zendy

Brandon T. Larsen | Zendy; Aaron H. Bubolz | Zendy; Suelhem A. Mendoza | Zendy; Kirkwood A. Pritchard | Zendy; David D. Gutterman | Zendy

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Bradykinin-Induced Dilation of Human Coronary Arterioles Requires NADPH Oxidase–Derived Reactive Oxygen Species

Author(s) -

Brandon T. Larsen,

Aaron H. Bubolz,

Suelhem A. Mendoza,

Kirkwood A. Pritchard,

David D. Gutterman

Publication year - 2009

Publication title -

arteriosclerosis thrombosis and vascular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.007

H-Index - 270

eISSN - 1524-4636

pISSN - 1079-5642

DOI - 10.1161/atvbaha.108.169367

Subject(s) - nadph oxidase , apocynin , superoxide , bradykinin , chemistry , nox1 , reactive oxygen species , nox4 , vasodilation , pharmacology , oxidase test , agonist , biochemistry , receptor , endocrinology , enzyme , biology

Hydrogen peroxide (H2O2) is an endothelium-derived hyperpolarizing factor in human coronary arterioles (HCAs). H2O2 mediates bradykinin (BK)-induced vasodilation and reduces bioavailability of epoxyeicosatrienoic acids (EETs); however, the cellular and enzymatic source of H2O2 is unknown.

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