Bleecker E R
Am J Med. 1986 Nov 14;81(5A):93-102. doi: 10.1016/0002-9343(86)90470-5.
Although primary neural control of airway function is through parasympathetic pathways, more recent evidence indicates that there are important adrenergic and non-adrenergic, non-cholinergic neural mechanisms that may also influence respiratory function. The parasympathetic nervous system component includes neural receptors in the airways as well as afferent and efferent pathways that travel in the vagus nerves. Afferent vagal sensory receptors mediate the response to irritant or rapidly adapting receptor activation, Hering-Breuer, and the unmyelinated "C" fibers or "J" receptor pathways. The motor component of the parasympathetic nervous system has several important functions that regulate tone in normal system has several important functions that regulate tone in normal and obstructed airways. These pathways affect the following respiratory structures: bronchial smooth muscle; the mucociliary system; the larynx; and the nose. Finally, the parasympathetic nervous system may play a role in some species in the control of breathing and in the hyperpneic responses associated with airflow obstruction. In addition to cholinergic neural mechanisms, bronchomotor tone may also be influenced by adrenergic mechanisms and non-adrenergic, non-cholinergic neural pathways. Although there is minimal innervation of the airways by the sympathetic nervous system, there is ample evidence that beta-adrenoreceptors are present on bronchial smooth muscle. Beta-receptor stimulation not only relaxes airway smooth muscle, but also inhibits mediator release from mast cells in the airways and may alter vascular permeability. Alpha-adrenoreceptors are found in human airways and stimulation of these receptors causes bronchoconstriction. Although the importance of alpha-adrenoreceptors has been questioned, recent evidence suggests that alpha stimulation may play a role in cold air- and exercise-induced asthma. Finally, non-adrenergic, non-cholinergic nerves have been shown to cause relaxation of human airways in in vivo studies. There is increasing evidence that vasoactive intestinal peptide and peptide histidine methanol are the mediators of these responses. More recently, other neuropeptides (substance P, neurokinin A, and calcitonin gene-related peptide) have been localized in nerves in airways. These cause bronchoconstriction in vitro and may be released from afferent nerve terminals by an axon reflex. Although the precise role of these substances in controlling airway tone and bronchial secretions in humans is not fully understood, they may have important modulatory effects on the neural control of airway function.
虽然气道功能的主要神经控制是通过副交感神经通路，但最近的证据表明，存在重要的肾上腺素能和非肾上腺素能、非胆碱能神经机制，它们也可能影响呼吸功能。副交感神经系统组成部分包括气道中的神经受体以及在迷走神经中穿行的传入和传出通路。迷走神经传入感觉受体介导对刺激物或快速适应受体激活、黑林 - 布雷尔反射以及无髓鞘的“C”纤维或“J”受体通路的反应。副交感神经系统的运动成分具有多种重要功能，可调节正常和阻塞气道的张力。这些通路影响以下呼吸结构：支气管平滑肌；黏液纤毛系统；喉部；以及鼻腔。最后，副交感神经系统在某些物种中可能在呼吸控制以及与气流阻塞相关的呼吸增强反应中发挥作用。除了胆碱能神经机制外，支气管运动张力还可能受肾上腺素能机制和非肾上腺素能、非胆碱能神经通路的影响。虽然交感神经系统对气道的支配极少，但有充分证据表明支气管平滑肌上存在β - 肾上腺素能受体。β受体刺激不仅可松弛气道平滑肌，还能抑制气道中肥大细胞释放介质，并可能改变血管通透性。α - 肾上腺素能受体存在于人类气道中，刺激这些受体可导致支气管收缩。尽管α - 肾上腺素能受体的重要性受到质疑，但最近的证据表明α刺激可能在冷空气和运动诱发的哮喘中起作用。最后，在体内研究中已表明非肾上腺素能、非胆碱能神经可导致人类气道松弛。越来越多的证据表明血管活性肠肽和肽组氨酸甲硫氨酸是这些反应的介质。最近，其他神经肽（P物质、神经激肽A和降钙素基因相关肽）已定位在气道神经中。它们在体外可引起支气管收缩，并可能通过轴突反射从传入神经末梢释放。虽然这些物质在控制人类气道张力和支气管分泌物的确切作用尚未完全了解，但它们可能对气道功能的神经控制具有重要的调节作用。
