Human coronary arteriolar dilation to bradykinin depends on membrane hyperpolarization: Contribution of nitric oxide and Ca2+-activated K+ channels

Circulation

Volumn 99, Issue 24, 1999, Pages 3132-3138

  Miura, Hiroto ^a   Liu, Yanping ^b   Gutterman, David D ^b  

^a UNIVERSITY OF IOWA   (United States)

^b MEDICAL COLLEGE OF WISCONSIN   (United States)

Author keywords

Bradykinin; Endothelin; Nitric oxide; Potassium; Vasodilation

Indexed keywords

APAMIN; BRADYKININ; CALCIUM; CHARYBDOTOXIN; ENDOTHELIN 1; ENDOTHELIUM DERIVED HYPERPOLARIZING FACTOR; GLIBENCLAMIDE; N(G) NITROARGININE METHYL ESTER; NITRIC OXIDE; NITRIC OXIDE SYNTHASE; NITROPRUSSIDE SODIUM; POTASSIUM CHANNEL; PROSTAGLANDIN SYNTHASE;

ARTICLE; BLOOD VESSEL DIAMETER; BLOOD VESSEL REACTIVITY; BLOOD VESSEL TONE; CHANNEL GATING; CONTROLLED STUDY; CORONARY ARTERY DILATATION; CORONARY VASCULAR RESISTANCE; ENZYME INHIBITION; HEART MUSCLE ISCHEMIA; HUMAN; HUMAN TISSUE; HYPERPOLARIZATION; MEMBRANE POLARIZATION AND DEPOLARIZATION; MICROVASCULATURE; PRIORITY JOURNAL; VASCULAR SMOOTH MUSCLE;

EID: 0033594946     PISSN: 00097322     EISSN: None     Source Type: Journal    
DOI: 10.1161/01.CIR.99.24.3132     Document Type: Article

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