Abstract
Ischemic heart disease and myocardial infarction continue to be leading causes of cardiovascular morbidity and mortality. Activation of opioid, adenosine, bradykinin, adrenergic and other G-protein coupled receptors has been found to be cardioprotective. κ- and/or δ-opioid receptor activation is involved in direct myocardial protection, while the role of µ-opioid receptors seems less clear. In addition, differential affinities to the three opioid-receptor subtypes by various agonists and cross-talk among different G-protein coupled receptors render conclusions regarding opioid-mediated cardioprotection challenging. The present review will focus on the protective effects of endogenously released opioid peptides as well as exogenously administered opioids such as morphine, fentanyl, remifentanil, butorphanol, and methadone against myocardial ischemia/reperfusion injury. Receptor heterodimerization and cross-talk as well as interactions with other cardioprotective techniques will be discussed. Implications for opioid-induced cardioprotection in humans and for future drug development to improve myocardial salvage will be provided.
Keywords: Butorphanol, cross-talk, enkephalin, fentanyl, heterodimerization, ischemia-reperfusion injury, opioid receptors, methadone, morphine, myocardial, remifentanil.
Current Pharmaceutical Design
Title:Opioid-induced Cardioprotection
Volume: 20 Issue: 36
Author(s): Katsuya Tanaka, Judy R. Kersten and Matthias L. Riess
Affiliation:
Keywords: Butorphanol, cross-talk, enkephalin, fentanyl, heterodimerization, ischemia-reperfusion injury, opioid receptors, methadone, morphine, myocardial, remifentanil.
Abstract: Ischemic heart disease and myocardial infarction continue to be leading causes of cardiovascular morbidity and mortality. Activation of opioid, adenosine, bradykinin, adrenergic and other G-protein coupled receptors has been found to be cardioprotective. κ- and/or δ-opioid receptor activation is involved in direct myocardial protection, while the role of µ-opioid receptors seems less clear. In addition, differential affinities to the three opioid-receptor subtypes by various agonists and cross-talk among different G-protein coupled receptors render conclusions regarding opioid-mediated cardioprotection challenging. The present review will focus on the protective effects of endogenously released opioid peptides as well as exogenously administered opioids such as morphine, fentanyl, remifentanil, butorphanol, and methadone against myocardial ischemia/reperfusion injury. Receptor heterodimerization and cross-talk as well as interactions with other cardioprotective techniques will be discussed. Implications for opioid-induced cardioprotection in humans and for future drug development to improve myocardial salvage will be provided.
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Cite this article as:
Tanaka Katsuya, Kersten R. Judy and Riess L. Matthias, Opioid-induced Cardioprotection, Current Pharmaceutical Design 2014; 20 (36) . https://dx.doi.org/10.2174/1381612820666140204120311
DOI https://dx.doi.org/10.2174/1381612820666140204120311 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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