Abstract
The action of acetylcholine (ACh) on sheep tracheal epithelium has been investigated. ACh increases transiently the short-circuit current (ISC). The same response is obtained in tissues in which the apical membrane has been permeabilized with amphotericin B in the presence of a potassium gradient. Microelectrode studies show that the majority of tracheal epithelial cells depolarize as the apical fractional resistance decreases on application of ACh. These results, together with the finding that bumetanide decreases the initial ACh-induced ISC increase, are consistent with an initial activation by ACh of apical Cl channels and basolateral K+ channels. Following the initial increase, ISC declines to values lower than in control conditions both in untreated and in amphotericin-permeabilized tissues, suggesting that the basolateral K+ conductance falls during this phase. The late decrease in ISC induced by ACh is significantly reduced in tissues pretreated with amiloride, suggesting that the apical Na+ channels are also involved in this response. ACh abolishes the net Na+ absorption by decreasing the mucosal to serosal Na+ flux. This effect is possibly a result of a down-regulation of apical Na+ channels and basolateral K+ channels.