Cardiovascular effects and underlying mechanisms of adenosine and its analogues

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.