Modulation of ATP-sensitive K+ channels in rabbit ventricular myocytes by adenosine A1 receptor activation.
Modulation of ATP-sensitive K+ channels in rabbit ventricular myocytes by adenosine A1 receptor activation.
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通过腺苷 A1 受体激活调节兔心室肌细胞中 ATP 敏感 K 通道。
DOI：
10.1152/ajpheart.1997.272.1.h325
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Y. Earm
中科院分区：
文献类型：
--
作者：
E. Kim;J. Han;W. Ho;Y. Earm
采用膜片钳技术研究腺苷对离体兔心室肌细胞ATP敏感性K（KATP）通道活性的调节作用。在一个由外向外的补丁暴露于鸟苷5 '-三磷酸和ATP在细胞内表面，外部腺苷刺激KATP通道活性。在暴露于外部腺苷的由内而外的贴片中，ATP降低KATP通道活性，鸟苷5 '-三磷酸刺激KATP通道活性。鸟苷5 '-O-（3-硫代三磷酸）导致KATP通道活性的逐渐增加，即使在没有腺苷的情况下。当肌细胞与百日咳毒素或8-环戊基-1，3-二丙基黄嘌呤预孵育时，腺苷A1受体激活未能激活KATP通道。开放和关闭的时间分布的分析表明，腺苷A1受体激活增加爆发持续时间和减少爆发间持续时间。在ATP的剂量-反应关系中，腺苷A1受体激活将KATP通道的半数最大抑制从70 μ M转移到241 μ M。
The objective of the present study was to characterize the role of adenosine in the regulation of ATP-sensitive K (KATP) channel activity in isolated rabbit ventricular myocytes using the patch-clamp technique. In an outside-out patch exposed to guanosine 5'-triphosphate and ATP at the intracellular surface, external adenosine stimulated KATP channel activity. In an inside-out patch exposed to external adenosine, ATP reduced KATP channel activity and guanosine 5'-triphosphate stimulated KATP channel activity. Guanosine 5'-O-(3-thiotriphosphate) resulted in a gradual increase of KATP channel activity even in the absence of adenosine. When myocytes were preincubated with pertussis toxin or 8-cyclopentyl-1,3-dipropylxanthine, adenosine A1 receptor activation failed to activate the KATP channel. Analysis of the open and closed time distributions showed that adenosine A1 receptor activation increased burst duration and decreased interburst duration. In a dose-response relationship for ATP, adenosine A1 receptor activation shifted the half-maximal inhibition of the KATP channel from 70 to 241 microM.