Abstract
We investigated the direct action of angiotensin II (Ang II) on myocardial conduction and transmembrane action potential immediately after reoxygenation. MethodAfter superfusion in a simulated ischemic solution, ventricular papillary muscle preparations of rat heart were washed with oxygenated Tyrode solution containing Ang II, Ang II plus CV-11974 (an AT1 receptor blocker), or Ang II plus 5-hydroxydecanoic acid (mito-KATP blocker), under rapid electrical stimulation (RES) for 60s. ResultsIn the control experiments, the incidence of conduction delay and block was the highest within the first 10s, and subsequently, 1:1 conduction was established after 40s. Ang II significantly enhanced the 2:1 conduction block during the later phase of RES (40–60s after reoxygenation). This effect of Ang II was abolished by either CV-11974 (P<0.001) or 5-HD (P<0.001). ConclusionRES-induced conduction delay and block immediately after reoxygenation were accelerated by Ang II, which could be relevant to the maintenance of reperfusion arrhythmias. The mito-KATP channel may participate in the mechanism underlying this phenomenon.
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