Costello R W, Jacoby D B, Fryer A D
Department of Medicine, University of Liverpool, UK.
Thorax. 1998 Jul;53(7):613-6. doi: 10.1136/thx.53.7.613.
In the lungs neuronal M2 muscarinic receptors limit acetylcholine release from postganglionic cholinergic nerves. These inhibitory M2 receptors are dysfunctional in antigen challenged guinea pigs and in humans with asthma which leads to an increase in vagally mediated hyperreactivity. In vitro, eosinophil products act as allosteric antagonists at neuronal M2 muscarinic receptors. In vivo, displacing or neutralising MBP preserves neuronal M2 muscarinic receptor function and prevents hyperreactivity. Thus, there is good evidence from animal studies that after antigen challenge pulmonary M2 muscarinic receptors become dysfunctional because MBP inhibits their function. Loss of function of pulmonary neuronal M2 muscarinic receptors has also been reported in patients with asthma, although the clinical significance of this dysfunction and the mechanisms underlying it are not yet established.
在肺中，神经元M2毒蕈碱受体限制节后胆碱能神经释放乙酰胆碱。这些抑制性M2受体在抗原攻击的豚鼠和哮喘患者体内功能失调，这会导致迷走神经介导的高反应性增加。在体外，嗜酸性粒细胞产物作为神经元M2毒蕈碱受体的变构拮抗剂。在体内，置换或中和髓磷脂碱性蛋白（MBP）可保留神经元M2毒蕈碱受体功能并预防高反应性。因此，动物研究有充分证据表明，抗原攻击后肺M2毒蕈碱受体功能失调是因为MBP抑制了它们的功能。哮喘患者也有肺神经元M2毒蕈碱受体功能丧失的报道，尽管这种功能失调的临床意义及其潜在机制尚未明确。
