δ-Opioid receptor as a target for the creation of peptide drugs that increase cardiac resistance to reperfusion

Abstract

An analysis of published data and the results of our own studies showed that activation of peripheral δ2-opioid receptor (δ2-OR) increases cardiac tolerance to reperfusion. It has been established that this δ2-OR is localized in cardiomyocytes. Endogenous opioids are not involved in the regulation of cardiac resistance to reperfusion in non-adapted rats. The infarct-limiting effect of δ2-OR agonist deltorphin II depends on the activation of following protein kinases: PKCδ, ERK1/2, PI3K, PCG. SarcKATP channel and MPT pore are hypothetical end effectors of the cardioprotective effect of deltorphin II.