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内皮素和ATP敏感性钾通道介导缺氧所致家兔窦房结起搏细胞的电生理效应

张朝, 孙光启, 李玉龙, 何瑞荣

(河北医科大学基础医学研究所生理室，石家庄050017)

摘要

用细胞内微电极技术研究了ATP一敏感性钾(KATP)通道和内皮素(endothelin, ET)在缺氧所致窦房结起搏细胞负性频率中的作用，主要结果如下:(1)缺氧引起窦房结起搏细胞的RPF降低和APD缩短，这一效应随时间延长而加重。(2) KATP通道开放剂cromakalim浓度依赖性地对窦房结起搏细胞有负性频率作用，且明显缩短APD5o。该通道的阻断剂格列苯脉能部分阻断缺氧对起搏细胞的上述效应，表明缺氧效应中有KATP通道的参与。(3) ET-1可显著加重缺氧所致的RPF降低，使起搏细胞停跳时间前移;而以ET*受体阻断剂BQ-123预处理窦房结标本后，则能有效地缓解缺氧对起搏细胞的效应，提示内源性ET-1的释放在缺氧效应中的作用。上述结果表明，缺氧所致起搏细胞的负性频率作用和APD缩短，与KATP通道的激活和内源性ET-1的释放有关。

关键词： 缺氧; 窦房结; K_(ATP)通道; 内皮素; Cromakalim; 格列苯服; BQ-123; 电生理

ENDOTHELIN AND ATP-SENSITIVE POTASSIUM CHANNEL MEDIATE ELECTROPHYSIOLOGICAL CHANGES INDUC BY HYPOXIA IN RABBIT SINOATRIAL NODEED

ZHANG ZHAO, SUN GUANG-QI, LI YU-LONG, HE RUI-RONG

Department of Physiology, Institute of Basic Medicine, Hebei Medical Unvwsity, Shijiax} 050017)

Abstract

The role of ET and K_(ATP) channel in hypoxia-induced negative chronotropic effect of pacemaker cells in rabbit sinoatrial node was studied with intracellular microelectrode technique. The results obtained were as follows:(1)Hypoxia produced a progressive decrease in the velocity of diastolic depolarization (VDD) of pacemaker cells resulting in a reduced rate of pacemaker firing (RPF)，and induced a decrease in APD，especially
APD5o. (2) K_(ATP) channel opener cromakalim markedly induced a negative chronotropic effect in a concentration-dependent manner and significantly shortened APD5o. K_(ATP )channel blocker glibenclamide alleviated.the effects of hypoxia on pacemaker cells，thereby suggesting the involvement of KATP channel in the hypoxia-induced effects.(3) By superfusion of ET-1，the hypoxia-induced decrease in RPF was remarkably potentiated and the occurrence of pacemaker arrest was shifted to an earlier time. The h3,poxia-induced effects could be effectively attenuated after pretreatment with BQ-123，implying the role of endogenous ET-1 release in hypoxia-induced effects. It is conclud
ed that the negative chronotropic effect and the decrease in APD induced by hypoxia may be attributed to the activation of K_(ATP)channel and the release of endogenous ET.

Key words: Hypoxia; sinoatrial node;KprP channel;Endothelin; cromakalim;glibenclamide; BQ123;electrophysiology

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引用本文：

张朝, 孙光启, 李玉龙, 何瑞荣. 内皮素和ATP敏感性钾通道介导缺氧所致家兔窦房结起搏细胞的电生理效应[J]. 生理学报 1996; 48 (3): .

ZHANG ZHAO, SUN GUANG-QI, LI YU-LONG, HE RUI-RONG. ENDOTHELIN AND ATP-SENSITIVE POTASSIUM CHANNEL MEDIATE ELECTROPHYSIOLOGICAL CHANGES INDUC BY HYPOXIA IN RABBIT SINOATRIAL NODEED . Acta Physiol Sin 1996; 48 (3): (in Chinese with English abstract).