Neurokinin3 receptor regulation of the airways

Neurokinin3 receptor regulation of the airways
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DOI:
10.1016/j.vph.2005.08.031
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发表时间:
2006-10-01
影响因子:
4
通讯作者:
Canning, Brendan J.
Canning, Brendan J.
中科院分区:
医学2区
文献类型:
--
作者:
Canning, Brendan J.

文献摘要

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神经蛋白(3)(NK3)受体可能主要通过作用于神经来调节气道。在外周,气道副交感神经节神经元在NK3受体激活后去极化,从而促进突触传递。这种效应可能解释了过度的副交感反射效应(如气道平滑肌收缩、血管扩张、粘液分泌)与哮喘和慢性阻塞性肺疾病(COPD)相关。在中枢神经系统(CNS)中,NK3受体的激活可能调节气道迷走神经传入中继神经元,使它们对含有谷氨酸的传入神经的平行输入产生高反应。这一过程类似于调节躯体组织痛觉过敏和疼痛的中枢致敏过程。在中枢神经系统和气道中,NK3受体可能被P物质和/或神经激肽A (NKA)激活,这两种物质都是NK3受体的完全激动剂,因为几乎没有证据表明气道神经表达神经激肽B (NKB)。关于NK3受体在气道中的其他潜在调控位点(如脉管系统、气道平滑肌、上皮、粘液腺)的证据要么是不确定的,要么是相互矛盾的。(c) 2006爱思唯尔公司版权所有。
Neurokmin(3) (NK3) receptors may regulate the airways primarily through actions on the nerves. In the periphery, airway parasympathetic ganglia neurons are depolarized following NK3 receptor activation resulting subsequently in the facilitation of synaptic transmission. Such an effect may account for the excessive parasympathetic reflex effects (e.g. airway smooth muscle contraction, vascular engorgement, mucus secretion) associated with asthma and chronic obstructive pulmonary disease (COPD). In the central nervous system (CNS), NK3 receptor activation may regulate airway vagal afferent relay neurons, rendering them hyperresponsive to parallel inputs from glutamate containing afferent nerves. This process is analogous to the process of central sensitization regulating hyperalgesia and pain in somatic tissues. In both the CNS and in the airways, NK3 receptors are likely activated by either substance P and/or neurokinin A (NKA), both of which are full agonists at NK3 receptors, as there is little evidence that airway nerves express neurokinin B (NKB). Evidence for other potential sites of regulation by NK3 receptors in the airways (e.g. vasculature, airway smooth muscle, epithelium, mucus glands) is either inconclusive or conflicting. (c) 2006 Elsevier Inc. All rights reserved.