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

Inhibitors of Cl- and HCO3- 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. Mel. Physiol. 16): L372-L377, 1997]. The present study quantified contribut ions of Cl- and HCO3- transport to volume and composition of acetylcholine- induced liquid secretion by airway epithelium. When distal bronchi were exc ised from 33 pigs and treated with 10 mu M acetylcholine, the airways secre ted 13.4 +/- 0.7 mu l . cm(-2).h(-1). Bumetanide (10 mu M) pretreatment red uced acetylcholine-induced liquid and Cl- secretion rates by similar to 70% , but HCO3- secretion fell by only 40%. Dimethylamiloride (DMA; 100 mu M) p retreatment reduced Cl- secretion rates by similar to 15%, but HCO3- secret ion 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 ac etylcholine-induced Liquid secretion in distal bronchi is dependent on Cl- secretion. Most of the remaining response is driven by HCO3- secretion. We speculate that the principal source of this liquid is submucosal glands. Cr ossover inhibition of bumetanide on HCO3- secretion and DMA on Cl- secretio n implies modulation of anion secretion secondary to changes in cell electr olyte composition.