TRPV1 activation is involved in the cardioprotection of remote limb ischemic postconditioning in ischemia-reperfusion injury rats

Limb remote ischemic postconditioning (RIPostC) has been proved to be a safe and effective measurement of cardioprotection against ischemia-reperfusion injury. But what bridges the remote organ insult and the cardioprotective effect in heart remains to be elucidated. This study aimed to found that whether TRPV1 may mediate the cardioprotective effect from remote organ to heart and the role of CGRP and SP in this process. We found that RIPostC effectively ameliorated cardiac ischemia/reperfusion injury in terms of limiting infarct size, lowering CK and cTnI release and improving cardiac function. In addition, these cardioprotective effects could be significantly abolished by inhibition of either CGRP or SP receptors with corresponding antagonists (CGRP8-37 for CGRP and RP-67580 for SP) injected before reperfusion. Besides, RIPostC resulted in significantly increase in the levels of CGRP and SP in plasma and hearts, as well as the levels and mRNA expression of CGRP and SP in DRG. The increase in CGRP and SP levels in plasma and hearts were markedly inhibited by TRPV1 receptor antagonist capsazepine. These findings indicate that limb remote ischemic postconditioning could attenuate cardiac ischemia/reperfusion injury in rats, and the cardioprotective mechanism is via TRPV1-mediated upregulation of CGRP and SP, which could subsequently act on their corresponding receptors in heart tissue.