INCREASED PRODUCTION OF NITRIC-OXIDE IN CORONARY-ARTERIES DURING CONGESTIVE-HEART-FAILURE

被引:80
作者
OMURCHU, B
MILLER, VM
PERRELLA, MA
BURNETT, JC
机构
[1] MAYO CLIN & MAYO FDN,DEPT SURG,DIV CARDIOVASC DIS,CARDIORENAL RES LAB,ROCHESTER,MN 55905
[2] MAYO CLIN & MAYO FDN,DEPT PHYSIOL & BIOPHYS,ROCHESTER,MN 55905
关键词
ENDOTHELIUM; VASODILATATION; ADRENERGIC FUNCTION; CORONARY BLOOD FLOW; GUANINE NUCLEOTIDE-BINDING REGULATORY PROTEINS;
D O I
10.1172/JCI116940
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Experiments were designed to determine whether a heterogeneity of endothelium-dependent relaxations in arteries from different vascular beds exists in experimental congestive heart failure (CHF) and to determine the mediators of those responses. CHF was produced in dogs by rapid ventricular pacing for 15 d. Rings of coronary, femoral, and renal arteries with and without endothelium from control and CHF dogs were suspended in organ chambers for measurement of isometric force. In arteries contracted with prostaglandin F-2 alpha, endothelium-dependent relaxations to BHT 920 (an alpha(2)-adrenergic agonist) were increased in coronary arteries from dogs with CHF (maximal relaxation: control -15+/-9% vs CHF -92+/-5%; n = 5-6; P < 0.05), with a modest enhancement in renal arteries. Relaxations to adenosine diphosphate and the calcium ionophore were unchanged. Relaxations to BHT 920 in CHF were reduced by N-G monomethyl-L-arginine (L-NMMA) and pertussis toxin but not by indomethacin. These data suggest that endothelium-dependent relaxations are affected heterogeneously in CHF. The enhanced response to alpha(2)-adrenergic agonists in the coronary artery is mediated by nitric oxide through a mechanism sensitive to inhibition by pertussis toxin. This selective increase in endothelium-dependent relaxations in the coronary artery may contribute to preserving coronary blood flow during CHF.
引用
收藏
页码:165 / 171
页数:7
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