首页> 外文期刊>Endothelium: Journal of endothelial cell research >Effects of beta-endorphin on endothelial/monocytic endothelin-1 and nitric oxide release mediated by mu1-opioid receptors: a potential link between stress and endothelial dysfunction?
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Effects of beta-endorphin on endothelial/monocytic endothelin-1 and nitric oxide release mediated by mu1-opioid receptors: a potential link between stress and endothelial dysfunction?

机译:β-内啡肽对mu1-阿片受体介导的内皮/单核细胞内皮素-1和一氧化氮释放的影响:应激和内皮功能障碍之间的潜在联系?

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Observations have been made linking the presence of psychosocial factors associated with elevated beta-endorphin concentrations with atherosclerosis. In this study, the authors assume an important role of the stress hormone beta-endorphin in several mechanisms that contribute to a dysbalance of human endothelial and monocytic endothelin (ET)-1 and nitric oxide (NO) release, mediated by mu1-opioid receptors. ET-1 and NO release were quantified via enzyme-linked immunosorbent assay (ELISA) or fluorometrically. mu1-Opioid receptors were identified by polymerase chain reaction (PCR) after stimulation with beta-endorphin. beta-Endorphin significantly increased endothelial and monocytic ET-1 release. The effect was mediated by mu1-opioid receptors and abolished by naloxonazine, a selective mu1-opioid receptor antagonist. In contrast, NO release was decreased under the influence of beta-endorphin. mu1-Opioid receptors on human monocytes and endothelial cells mediated a beta-endorphin-induced stimulation of ET-1 release, whereas NO release was decreased. Thus, the authors hypothesize a role of beta-Endorphin in the pathogenesis of stress-induced endothelial dysfunction through peripherally circulating beta-endorphin, which may offset the balance of vasoactive mediators, leading to an unopposed vasoconstriction. The data may also provide a new concept of mu1-opioid receptor antagonists, preventing beta-endorphin-induced disorders of vascular biology.
机译:有人将与β-内啡肽浓度升高有关的社会心理因素与动脉粥样硬化联系起来。在这项研究中,作者认为应激激素β-内啡肽在多种机制中起着重要作用,这些机制由mu1-阿片受体介导的人内皮和单核内皮素(ET)-1和一氧化氮(NO)释放失衡。 。 ET-1和NO的释放通过酶联免疫吸附测定(ELISA)或荧光定量。在β-内啡肽刺激后,通过聚合酶链反应(PCR)鉴定了mu1-阿片类药物受体。 β-内啡肽显着增加了内皮细胞和单核细胞ET-1的释放。这种作用是由阿片类鸦片受体介导的,而纳洛酮嗪则是一种选择性的阿片类鸦片受体拮抗剂。相反,在β-内啡肽的影响下NO释放减少。人单核细胞和内皮细胞上的mu1-阿片样物质受体介导了β-内啡肽诱导的ET-1释放刺激,而NO释放却减少了。因此,作者推测β-内啡肽通过周围循环的β-内啡肽在应激诱导的内皮功能障碍的发病机理中发挥作用,这可能抵消了血管活性介质的平衡,导致血管收缩无阻。数据也可能提供mu1-阿片受体拮抗剂的新概念,预防β-内啡肽引起的血管生物学疾病。

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