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δ-Opioid Receptor As a Molecular Target for Increasing Cardiac Resistance to Reperfusion in Drug Development

Abstract

An analysis of published data and the results of our own studies reveal that the activation of a peripheral δ-opioid receptor (δ-OR) increases the cardiac tolerance to reperfusion. It has been found that this δ-OR is localized in cardiomyocytes. Endogenous opioids are not involved in the regulation of cardiac resistance to reperfusion. The infarct-limiting effect of the δ-OR agonist deltorphin II depends on the activation of several protein kinases, including PKCδ, ERK1/2, PI3K, and PKG. Hypothetical end-effectors of the cardioprotective effect of deltorphin II are the sarcolemmal K channels and the MPT pore.

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