关键词: Cardioprotection Cardiovascular Endogenous opioids Opioid receptors

Mesh : Animals Humans Analgesics, Opioid / metabolism Cardiotonic Agents / pharmacology Heart / drug effects Opioid Peptides / metabolism Receptors, Opioid / metabolism

来  源:   DOI:10.1007/978-3-031-45493-6_19

Abstract:
The opioid system involves opioid receptors (OPRs) and endogenous opioid peptides.This chapter will focus on the distribution of OPRs in the cardiovascular system, the expression pattern in the heart, the activation by opioid peptides, and the effects of OPRs activation with potential relevance in cardiovascular performance. In the heart, OPRs are co-expressed with beta adrenergic receptors (β-ARs) in the G-protein-coupled receptor (GPCR) superfamily, functionally cross-talk with β-Ars and modify catecholamine-induced effects. They are involved in cardiac contractility, energy metabolism, myocyte survival or death, vascular resistance. The effects of the opioid system in the regulation of systemic circulation at both the central and peripheral level are presented. The pathways are discussed under physiological (i.e., aging) and pathological conditions (atherosclerosis, heart failure, essential hypertension, ischemic stress). Stimulation of OPRs not only inhibits cardiac excitation-contraction coupling, but also protects the heart against hypoxic and ischemic injury. An enhanced sensitivity to opioids of endocrine organs and neuronal systems is operative in hypertensive patients. The opioid system can be pharmacologically engaged to selectively mimic these responses via cardiac and nervous signaling. The clinical opportunities for the use of cardioprotective effects of opioids require future investigations to provide more specific details of the impact on cardiac performance and electrophysiological properties.
摘要:
阿片样物质系统涉及阿片样物质受体(OPR)和内源性阿片样肽。本章将重点介绍OPR在心血管系统中的分布,内心的表达模式,阿片类肽的激活,以及OPR激活与心血管表现潜在相关性的影响。在心中,OPR与G蛋白偶联受体(GPCR)超家族中的β肾上腺素能受体(β-ARs)共表达,与β-Ars的功能串扰并修饰儿茶酚胺诱导的作用。它们与心脏收缩有关,能量代谢,肌细胞存活或死亡,血管阻力。介绍了阿片样物质系统在中枢和外周水平调节体循环中的作用。途径在生理学(即,衰老)和病理状况(动脉粥样硬化,心力衰竭,原发性高血压,缺血性应激)。刺激OPR不仅抑制心脏兴奋-收缩耦合,还可以保护心脏免受缺氧和缺血性损伤。在高血压患者中,内分泌器官和神经系统对阿片类药物的敏感性增强。阿片样物质系统可以在药理学上参与以通过心脏和神经信号传导选择性地模拟这些反应。使用阿片类药物的心脏保护作用的临床机会需要进一步的研究,以提供对心脏性能和电生理特性的影响的更具体细节。
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