Killingsworth C R, Robinson N E
Department of Large Animal Clinical Sciences, Michigan State University, East Lansing 48824-1314.
Eur J Pharmacol. 1992 Jan 21;210(3):231-8. doi: 10.1016/0014-2999(92)90409-w.
The role of prejunctional inhibitory and facilitatory muscarinic receptors was investigated in cats with tracheal hyperresponsiveness to vagal stimulation. Intrathoracic airway caliber (total lung resistance (RL) and dynamic compliance (Cdyn] and the diameter of tracheal ring 4 were measured during vagal stimulation and local acetylcholine (ACh) injection before and after administration of the M1 receptor antagonist pirenzepine or the M2 receptor antagonist gallamine. The responses of tracheal ring 4, RL, and Cdyn to ACh were unaltered by gallamine or pirenzepine. Changes in RL and Cdyn during vagal stimulation were enhanced by gallamine, but the magnitude of tracheal constriction was unchanged. Vagally induced tracheal constriction was decreased by pirenzepine in hyperresponsive but not in control cats. The M2 receptors limit intrathoracic airway constriction, but a functional role for M2 receptors in the cervical trachea could not be demonstrated. However, these data suggest that M1 excitatory receptors may play a role in vagally mediated tracheal hyperreactivity.
在对迷走神经刺激有气管高反应性的猫中,研究了接头前抑制性和易化性毒蕈碱受体的作用。在给予M1受体拮抗剂哌仑西平或M2受体拮抗剂加拉明之前和之后,在迷走神经刺激和局部注射乙酰胆碱(ACh)期间,测量胸内气道口径(总肺阻力(RL)和动态顺应性(Cdyn))以及气管第4环的直径。加拉明或哌仑西平未改变气管第4环、RL和Cdyn对ACh的反应。加拉明增强了迷走神经刺激期间RL和Cdyn的变化,但气管收缩的程度未改变。哌仑西平使高反应性猫而非对照猫的迷走神经诱发的气管收缩减弱。M2受体限制胸内气道收缩,但无法证明M2受体在颈段气管中有功能作用。然而,这些数据表明M1兴奋性受体可能在迷走神经介导的气管高反应性中起作用。