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有证据表明 ,心脏细胞产生强腓肽和强腓肽类多肽 ,它们是kappa阿片受体 (κ OR)的激动剂。κ OR是心脏一种优势的阿片受体 ,其激活可改变在体和离体心脏的功能。在正常和病理情况下 ,内源性κ 阿片肽可能通过自分泌或旁分泌的方式调节心脏功能。心肌缺血是导致心脏功能紊乱的一个常见原因 ,主要表现为心肌功能减弱 ,心律失常及心肌梗塞等。心肌缺血时 ,交感神经发放增强 ,从而增加作功负荷及氧消耗量 ;而这又使缺血引发的状况更为恶化。机体抵抗缺血引发心肌损害 /心律失常的保护机制之一是抑制 β 肾上腺素受体 ( β AR)的兴奋。κ OR确实能抑制β AR的激动。这种抑制主要是由于GS蛋白受到抑制 ,也在较小程度上由于信息通路的腺苷酸环化酶的抑制。因为该种酶能通过对百日咳毒素敏感的G蛋白转导β AR的激动。另一保护心肌对抗缺血性损害的机制是预处理。预处理是指预先受到缺血等损伤使心脏对随后更严重的损伤产生较强的耐受能力。这种保护作用可以在预处理后即时产生 ,也可延至预处理后 1- 3天。在采用缺血或其产生的后果之一代谢抑制作为预处理而致的心脏保护中 ,κ OR参与媒介预处理的作用。用κ OR的特异性激动剂U5 0 488H激活κ OR (U5 0 488H药理性预处理 ,UP)可激活蛋白激酶C (PKC) ,开放ATP敏感
There is evidence that cardiac cells produce fibrinogen and fibrinoid polypeptides, which are agonists of the kappa opioid receptor (κ OR). κ OR is a dominant opioid receptor in the heart whose activation can alter the function of the heart in vivo and ex vivo. Under normal and pathological conditions, endogenous kappa-opioid peptides regulate cardiac function through autocrine or paracrine processes. Myocardial ischemia is a common cause of cardiac dysfunction, mainly manifested as myocardial dysfunction, arrhythmia and myocardial infarction. During myocardial ischemia, sympathetic release is increased, increasing work load and oxygen consumption, which in turn worsens the condition induced by ischemia. One of the mechanisms by which the body protects against ischemia-induced myocardial damage / arrhythmia is the inhibition of the excitability of the beta adrenergic receptor (AR). κ OR does inhibit the activation of β AR. This inhibition is mainly due to the inhibition of the GS protein, also to a lesser extent by the adenylyl cyclase inhibition of the signaling pathway. Because this enzyme can transduce the [beta] AR agonism through pertussis toxin-sensitive G protein. Another mechanism that protects the myocardium against ischemic damage is pretreatment. Pretreatment refers to pre-ischemic injury and other damage to the heart of the subsequent more serious damage resulting strong tolerance. This protective effect can be generated immediately after pretreatment, but also extended to 1-3 days after pretreatment. Κ-OR is involved in the role of vector preconditioning in cardioprotection using either ischemia or one of the consequences of metabolic inhibition as a pretreatment. Activation of κ-OR (U5 0488H pharmacological preconditioning, UP) with a specific agonist of κ-OR5 activates protein kinase C (PKC) and opens ATP-sensitive