EFFECTS OF ENDOTHELIN-1 ON ATP-SENSITIVE K+ CURRENT IN CARDIAC-CELLS

被引：0

作者：

KOBAYASHI, S ^{[1
]}

NAKAYA, H ^{[1
]}

TAKIZAWA, T ^{[1
]}

HARA, Y ^{[1
]}

KIMURA, S ^{[1
]}

SAITO, T ^{[1
]}

MASUDA, TY ^{[1
]}

机构：

[1] CHIBA UNIV,SCH MED,CTR NEUROBIOL & MOLEC IMMUNOL,DEPT PHARMACOL,CHUO KU,CHIBA 260,JAPAN

来源：

HEART AND VESSELS | 1995年

关键词：

ENDOTHELIN-1; ATP-SENSITIVE K+ CHANNEL; ACTION POTENTIAL DURATION; NICORANDIL;

D O I：

暂无

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Although plasma endothelin (ET) concentrations are known to increase in patients with acute myocardial infarction, the pathophysiological significance of the increased ET remains unclarified. In this study, the effects of ET on ATP-sensitive K+ channels were examined using conventional microelectrode and patch-clamp techniques. In isolated guinea-pig papillary muscles, endothelin-1 (ET-1, 30 nM) markedly increased the developed tension (DT) without affecting the action potential duration (APD). Nicorandil, a K+ channel opener, at a concentration of 1 mM shortened APD concominantly with a marked decrease in DT. Addition of ET-1, but not ET-3 (30 nM), partially reversed the nicorandil-induced decreases in APD and DT. In single ventricular myocytes, nicorandil (1 mM) increased a steady-state outward current which was sensitive to 1 mu M glibenclamide, suggesting that nicorandil activates the ATP-sensitive K+ current (I-K.ATP) ET-1 (30 nM) significantly inhibited I-K.ATP whereas ET-3 (30 nM) failed to affect I-K.ATP. These results suggest that ET-1 may inhibit I-K.ATP through the activation of ET(A) receptors. Since activation of the ATP-sensitive K+ channel is thought to play an important role in the protection of the ischemic myocardium, the inhibition of I-K.ATP by ET-1 may lead to the aggravation of myocardial injury, possibly due to an increase in transmembrane Ca2+ influx.

引用

页码：106 / 108

页数：3