The role of protein kinase C, ERK-kinase, NO-synthase, and katp-channels in the mechanism of antiarrhythmic effect of the kappa opioid, U-50,488, during short\term myocardial ischemia and reperfusion in vivo

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The selective ƒ1opioid receptor agonist, ()U50,488, increases cardiac tolerance to arrhythmogenic impact of short term ischemia and reperfusion via activation of NOsynthase, protein kinase C, and opening of KATPchannels. MEK1/2 and ERK1/2 kinases are not involved in the development of antiarrhythmic effect of ()U50,488.

Ischemia, reperfusion, heart, arrhythmias, opioid receptors, protein kinases

Короткий адрес: https://sciup.org/14919831

IDR: 14919831

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