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缓激肽对伤害感受器的兴奋和致敏作用:我们了解多少?

Excitation and sensitization of nociceptors by bradykinin: what do we know?

作者信息

Mizumura Kazue, Sugiura Takeshi, Katanosaka Kimiaki, Banik Ratan K, Kozaki Yasuko

机构信息

Division of Stress Recognition and Response, Department of Neuroscience II, Research Institute of Environmental Medicine, Nagoya University, Nagoya 464-8601, Japan.

出版信息

Exp Brain Res. 2009 Jun;196(1):53-65. doi: 10.1007/s00221-009-1814-5. Epub 2009 Apr 26.

Abstract

Bradykinin is an endogenous nonapeptide known to induce pain and hyperalgesia to heat and mechanical stimulation. Correspondingly, it excites nociceptors in various tissues and sensitizes them to heat, whereas sensitizing effect on the mechanical response of nociceptors is not well established. Protein kinase C and TRPV1 contribute to the sensitizing mechanism of bradykinin to heat. In addition, TRPA1 and other ion channels appear to contribute to excitation caused by bradykinin. Finally, prostaglandins sensitize bradykinin-induced excitation in normal tissues by restoring desensitized responses due to the inhibition of protein kinase A.

摘要

缓激肽是一种内源性九肽,已知其可诱发疼痛以及对热和机械刺激产生痛觉过敏。相应地,它能兴奋各种组织中的伤害感受器并使其对热敏感,而对伤害感受器机械反应的敏化作用尚未完全明确。蛋白激酶C和瞬时受体电位香草酸亚型1(TRPV1)参与缓激肽对热的敏化机制。此外,瞬时受体电位锚蛋白1(TRPA1)和其他离子通道似乎也参与缓激肽引起的兴奋过程。最后,前列腺素通过恢复因蛋白激酶A受抑制而脱敏的反应,使缓激肽在正常组织中诱导的兴奋作用敏感化。

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