Generic placeholder image

Current Pharmaceutical Design

Eiditor-in-Chief

ISSN (Print): 1381-6128
ISSN (Online): 1873-4286

Opioid-induced Cardioprotection

Author(s): Katsuya Tanaka, Judy R. Kersten and Matthias L. Riess

Volume 20 , Issue 36 , 2014

Page: [5696 - 5705] Pages: 10

DOI: 10.2174/1381612820666140204120311

Price: $58

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.


Rights & Permissions Print Export Cite as
Article Metrics
41
Related Journals
Related eBooks
Related Articles
© 2019 Bentham Science Publishers