Acetylcholine-induced liquid secretion by bronchial epithelium: role of Cl− and HCO 3 − transport

Abstract

Inhibitors of Cl− and[Formula: see text] 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 Cl− and[Formula: see text] 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 ± 0.7 μl ⋅ cm−2 ⋅ h−1. Bumetanide (10 μM) pretreatment reduced acetylcholine-induced liquid and Cl− secretion rates by ∼70%, but [Formula: see text] secretion fell by only 40%. Dimethylamiloride (DMA; 100 μM) pretreatment reduced Cl− secretion rates by ∼15%, but[Formula: see text] 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 Cl− secretion. Most of the remaining response is driven by[Formula: see text] secretion. We speculate that the principal source of this liquid is submucosal glands. Crossover inhibition of bumetanide on [Formula: see text]secretion and DMA on Cl−secretion implies modulation of anion secretion secondary to changes in cell electrolyte composition.