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.
|Original language||English (US)|
|Number of pages||3|
|Journal||Sheng li ke xue jin zhan [Progress in physiology]|
|State||Published - Jul 1996|
ASJC Scopus subject areas