Acetylcholine-induced liquid secretion by bronchial epithelium: role of Cl2 and HCO3

Trout, Laura, John T. Gatzy, and Stephen T. Ballard. Acetylcholine-induced liquid secretion by bronchial epithelium: role of Cl2 and HCO3 2 transport. Am. J. Physiol. 275 (Lung Cell. Mol. Physiol. 19): L1095–L1099, 1998.—Inhibitors of Cl2 and HCO3 2 secretion reduce acetylcholine-induced liquid, but not mucin, secretion by bronchial submucosal glands [S. K. Inglis, M. R. Corboz, A. E. Taylor, and S. T. Ballard. Am. J. Physiol. 272 (Lung Cell. Mol. Physiol. 16): L372–L377, 1997]. The present study quantified contributions of Cl2 and HCO3 2 transport to volume and composition of acetylcholine-induced liquid secretion by airway epithelium. When distal bronchi were excised from 33 pigs and treated with 10 μM acetylcholine, the airways secreted 13.4 6 0.7 μl ·cm22 ·h21. Bumetanide (10 μM) pretreatment reduced acetylcholine-induced liquid and Cl2 secretion rates by ,70%, but HCO3 2 secretion fell by only 40%. Dimethylamiloride (DMA; 100 μM) pretreatment reduced Cl2 secretion rates by ,15%, but HCO3 2 secretion fell 47%. DMA alone had little effect on liquid secretion. When airways were pretreated with both bumetanide and DMA, acetylcholine-induced liquid secretion was nearly abolished. We conclude that about three-fourths of acetylcholine-induced liquid secretion in distal bronchi is dependent on Cl2 secretion. Most of the remaining response is driven by HCO3 2 secretion. We speculate that the principal source of this liquid is submucosal glands. Crossover inhibition of bumetanide on HCO3 2 secretion and DMA on Cl2 secretion implies modulation of anion secretion secondary to changes in cell electrolyte composition.