Direct preconditioning of cultured chick ventricular myocytes. Novel functions of cardiac adenosine A2a and A3 receptors.
Direct preconditioning of cultured chick ventricular myocytes. Novel functions of cardiac adenosine A2a and A3 receptors.
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培养鸡心室肌细胞的直接预处理。
DOI：
10.1172/jci118976
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Liang,BT
中科院分区：
文献类型：
--
作者：
Strickler,J;Jacobson,KA;Liang,BT
在持续缺血前进行短暂缺血预处理可减少灌注心脏的梗死面积。建立了鸡心室肌细胞培养模型，探讨腺苷受体亚型在心脏预处理中的作用。在长时间缺氧之前，短暂的缺氧暴露，称为预处理缺氧，可以保护肌细胞免受长时间缺氧引起的损伤。CCPA激活腺苷A1受体或C1-IB-MECA激活A3受体可替代预处理缺氧并模拟预处理，在100 nM处效果最大。虽然1微米CGS21680对A2a受体的激活不能模拟预处理，但预处理缺氧时对其的刺激会减弱对缺氧损伤的保护作用。预处理缺氧时，选择性拮抗剂CSC （1 μ m）阻断A2a受体，可增强预处理的保护作用。硝苯地平阻断A2a受体介导的钙进入，消除了A2a激动剂诱导的预处理衰减。异丙肾上腺素、福斯可林和BayK 8644刺激钙的进入，也减弱了预处理。硝苯地平阻断了这些药物钙摄取的增加以及它们对预处理的减弱作用。本研究首次证明腺苷A3受体存在于心室肌细胞中，并能介导预适应的模拟。这些数据首次表明，A2a受体的激活可以拮抗腺苷的预处理作用，在预处理刺激期间增加钙的进入是一种新机制。
Preconditioning with brief ischemia before a sustained period of ischemia reduces infarct size in the perfused heart. A cultured chick ventricular myocyte model was developed to investigate the role of adenosine receptor subtypes in cardiac preconditioning. Brief hypoxic exposure, termed preconditioning hypoxia, prior to prolonged hypoxia, protected myocytes against injury induced by the prolonged hypoxia. Activation of the adenosine A1 receptor with CCPA or the A3 receptor with C1-IB-MECA can replace preconditioning hypoxia and simulate preconditioning, with a maximal effect at 100 nM. While activation of the A2a receptor by 1 microM CGS21680 could not mimic preconditioning, its stimulation during preconditioning hypoxia, however, attenuated the protection against hypoxia-induced injury. Blockade of A2a receptors with the selective antagonist CSC (1 microM) during preconditioning hypoxia enhanced the protective effect of preconditioning. Nifedipine, which blocked the A2a receptor-mediated calcium entry, abolished the A2a agonist-induced attenuation of preconditioning. Isoproterenol, forskolin, and BayK 8644, which stimulated calcium entry, also attenuated preconditioning. Nifedipine blocked the increase in calcium uptake by these agents as well as their attenuating effect on preconditioning. The present study provides the first evidence that the adenosine A3 receptor is present on ventricular myocytes and can mediate simulation of preconditioning. The data demonstrate, for the first time, that activation of the A2a receptor antagonizes the preconditioning effect of adenosine, with increased calcium entry during the preconditioning stimuli as a novel mechanism.
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DOI：
--
发表时间：
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期刊：
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影响因子：
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