Published online before print November 7, 2002, doi: 10.1161/01.RES.0000046003.14031.98
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© 2002 American Heart Association, Inc.
Integrative Physiology |
Peroxynitrite Inhibits Ca2+-Activated K+ Channel Activity in Smooth Muscle of Human Coronary Arterioles
From the Departments of Internal Medicine and Cardiovascular Center, Medical College of Wisconsin, and Zablocki VA Medical Center (Y.L., K.T., Q.C., H.L., D.G.), Milwaukee, Wis; and Cardiovascular Surgery Associates (L.K.), St Luke’s Medical Center, Milwaukee, Wis.
Correspondence to Yanping Liu, MD, PhD, Cardiovascular Center, Medical College of Wisconsin, 8701 Watertown Plank Rd, Milwaukee, WI 53226. E-mail ypliu{at}mcw.edu
We examined the hypothesis that ONOO-, a product of the interaction between superoxide (O2·-) and nitric oxide (NO), inhibits calcium-activated K+ (KCa) channel activity in vascular smooth muscle cells (VSMCs) of human coronary arterioles (HCAs), thereby reducing hyperpolarization-mediated vasodilation. HCAs were dissected from right atrial appendages. The interaction of ONOO- with microvessels was determined by immunohistochemistry using a nitrotyrosine antibody. Strong staining was observed in arteries exposed to authentic ONOO- or to sodium nitroprusside (SNP)+xanthine (XA)+xanthine oxidase (XO). Dilation to 10-8 mol/L bradykinin (BK) was abolished in vessels exposed to ONOO- (-2.5±8%; P<0.05) but not DC-ONOO- (65±8%). Reduced dilation to BK was also observed after application of XO and SNP. Dilation to NS1619 (KCa channel opener) was reduced in endothelial denuded arterioles treated with ONOO-. In isolated VSMCs, whole-cell peak K+ current density was reduced by ONOO- (control 65±15 pA/pF; ONOO- 42±9 pA/pF; P<0.05). Iberiotoxin had no further effect on whole-cell K+ current. In inside-out patches, ONOO- but not DC-ONOO- decreased open state probability (NPo) of KCa channel by 50±12%. O2·- generated by XA+XO had no effect on BK-induced dilation and NPo of KCa channels. These results suggest that ONOO-, but not O2·-, inhibits KCa channel activity in VSMCs possibly by a direct effect. This mechanism may contribute to impaired EDHF-mediated dilation in conditions such as ischemia/reperfusion where increased activity of NO synthase occurs in the presence of excess of O2·-.
Key Words: K+ channels • peroxynitrite • coronary circulation • vascular smooth muscle
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