Li Y L
Department of Physiology, Hebei Medical University, Shijia-zhuang.
Sheng Li Ke Xue Jin Zhan. 1996 Jul;27(3):238-40.
The present work was aimed to define the cardiovascular effects and underlying mechanisms of adenosine and its analogues. The results showed that (1) adenosine and 2-chloroadenosine could induce an initial increase in MAP mediated by the adenosine A2 receptors in carotid body chemoreceptor, and a subsequent decrease in MAP, being attributed to the adenosine A1 receptors in heart and A2 receptors in blood vessels; (2) N6-cyclopentyladenosine (CPA, a selective adenosine A1 receptor agonist) inhibited the electrophysiological activity of pacemaker cells in sinoatrial node; (3) CPA markedly attenuated the development of early afterdepolarization, delayed afterdepolarization and triggered activity induced by isoproterenol; (4) endogenous adenosine might play an important role in the generation of anoxic bradycardia; (5) activation of adenosine receptors along with an increase in adenosine receptor density during the course of ischemic preconditioning might provide the protective effect on the ischemic heart injury; (6) the cardiovascular effects of adenosine and its analogues were mainly mediated by activation of ATP sensitive K+ channels coupled to adenosine receptors.
本研究旨在确定腺苷及其类似物的心血管效应及潜在机制。结果表明：（1）腺苷和2-氯腺苷可先通过颈动脉体化学感受器中的腺苷A2受体介导使平均动脉压（MAP）升高，随后又因心脏中的腺苷A1受体和血管中的A2受体导致MAP降低；（2）N6-环戊基腺苷（CPA，一种选择性腺苷A1受体激动剂）抑制窦房结起搏细胞的电生理活性；（3）CPA显著减弱异丙肾上腺素诱导的早期后去极化、延迟后去极化及触发活动的发生；（4）内源性腺苷可能在缺氧性心动过缓的发生中起重要作用；（5）在缺血预处理过程中，腺苷受体的激活以及腺苷受体密度的增加可能对缺血性心脏损伤具有保护作用；（6）腺苷及其类似物的心血管效应主要通过与腺苷受体偶联的ATP敏感性钾通道的激活介导。
