腺苷及其衍生物的心血管效应和作用机制

Cardiovascular Effects and Underlying Mechanisms of Adenosine and Its Analogues

在实验中观察了腺苷及其衍生物的心血管效应和作用机制。结果表明：（１）腺苷和２－氯腺苷先引起由颈动脉体化学感受器内的Ａ２受体所中介的血压短暂升高，随之为心血管系统Ａ１和Ａ２受体中介的持久而明显的血压降低；（２）腺苷Ａ１受体激动剂环戊腺苷抑制窦房结起搏细胞的电生理活动；（３）环戊腺苷减弱异丙肾上腺素诱发的早发和迟发性后除极及触发电活动；（４）内源性腺苷参与无氧所致的心率减慢；（５）预缺血时腺苷受体的激活及腺苷受体数目增多对缺血心肌具有保护作用；（６）腺苷通过其受体激活ＡＴＰ敏感性钾通道。

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 increatse 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.