Synergistic modulation of ATP-sensitive K+ currents by protein kinase C and adenosine - Implications for ischemic preconditioning
Synergistic modulation of ATP-sensitive K+ currents by protein kinase C and adenosine - Implications for ischemic preconditioning
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DOI：
10.1161/01.res.78.3.443
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发表时间：
1996-03-01
影响因子：
20.1
通讯作者：
Marban, E
中科院分区：
文献类型：
--
作者：
Liu, YG;Gao, WD;Marban, E
缺血预处理涉及腺苷受体、蛋白激酶C（PKC）和ATP敏感性K+（K-ATP）通道的激活。本文研究了PKC激活和腺苷对离体兔心室肌细胞K-ATP电流（I-K，I-ATP）和动作电位的影响。预先暴露于PKC激活剂佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA，100 nmol/L）可显著增加对K-ATP通道开放剂吡那地尔（100 - 400 μ mol/L）的反应。PMA预处理可使0 mV时的I-K，I-ATP从0.55 ± 0.32增加到3.25 ± 0.47 nA（n=6，P
Ischemic preconditioning has been shown to involve the activation of adenosine receptors, protein kinase C (PKC), and ATP-sensitive K+ (K-ATP) channels. We investigated the effects of PKC activation and adenosine on K-ATP current (I-K,I-ATP) and action potentials in isolated rabbit ventricular myocytes. Responses to pinacidil (100 to 400 mu mol/L), an opener of K-ATP channels, were markedly increased by preexposure to the PKC activator phorbol 12-myristate 13-acetate (PMA, 100 nmol/L). I-K,I-ATP measured at 0 mV was increased by PMA pretreatment from 0.55+/-0.32 to 3.25+/-0.47 nA (n=6, P