Endogenous regulation of bronchomotor tone.
Endogenous regulation of bronchomotor tone.
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支气管运动张力的内源性调节。
DOI：
10.1164/ajrccm/137.5.1198
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Leff,AR
中科院分区：
文献类型：
--
作者：
Leff,AR
气道平滑肌反应是通过多种内源性介质以复杂的方式引起的。介导剂通过许多不同的机制在不同部位增强或抑制支气管张力。介质与神经、肌肉和循环血液成分或呼吸道肥大细胞之间发生相互作用。气道平滑肌张力进一步受到突触后介质-介质相互作用的调节。物质可以从远端部位通过血液循环到达其靶器官，如肾上腺素对气道平滑肌的作用，或者可以直接分泌到气道平滑肌上，如呼吸肥大细胞的分泌产物。最近的观察表明，一些介质引起气道收缩至少部分通过激活传出副交感神经和/或血小板。从邻近上皮或浸润白细胞直接分泌微量介质可能是气道高反应性的重要组成部分。补体和激肽释放酶级联之间的复杂相互作用已被引用为气道高反应性的可能机制。最终，支气管舒张张力通过平滑肌细胞收缩器的钙的可用性在突触后介导。磷脂酰肌醇系统在膜转导中的作用和环磷酸腺苷在调节平滑肌收缩的钙分布中的作用已经被暗示。已显示突触间隙远端的介体-介体相互作用以协同方式增加气道平滑肌收缩的力和持续时间。刺激诱发介质和神经递质分泌，其生理意义，以及这些相互作用的稳态基础设施是有前途的调查，需要进一步定义的领域。AM修订版DIS 1988; 137：1198-1216
Airway smooth muscle responses are elicited in a complex manner through a large variety of endogenous mediators. Mediators augment or inhibit bronchomotor tone at a variety of sites through numerous different mechanisms. Interactions occur among mediators and nerves, muscle, and circulating blood elements or respiratory mast cells. Airway smooth muscle tone further is regulated by postsynaptic mediator-mediator interactions. Substances may circulate through the blood from distal sites to reach their target organ, as with epinephrine in its effects on airway smooth muscle, or may be secreted directly onto airway smooth muscle, as with the secretory products of respiratory mast cells. Recent observations have indicated that some mediators elicit airway contraction at least in part by activating efferent parasympathetic nerves and/or platelets. Direct secretion of minute quantities of mediators from adjacent epithelium or from infiltrating leukocytes may be an essential component of airway hyperreactivity. Complex interactions between the complement and kallikrein cascades have been cited as possible mechanisms of airway hyperresponsiveness. Ultimately, bronchomotor tone is mediated postsynaptically by the availability of calcium to the contractile apparatus of the smooth muscle cell. A role for the phosphoinositide system in membrane transduction and for cyclic adenosine monophosphate in regulating calcium distribution for smooth muscle contraction has been implicated. Mediator-mediator interactions distal to the synaptic cleft have been shown to augment both force and duration of airway smooth muscle contraction in a synergistic fashion. The stimuli eliciting mediator and neurotransmitter secretion, their physiologic significance, and the homeostatic infrastructure of these interactions are areas of promising investigation that require further definition. AM REV RESPIR DIS 1988; 137: 1198-1216