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Am J Physiol Lung Cell Mol Physiol 274: L762-L766, 1998;
1040-0605/98 $5.00
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Vol. 274, Issue 5, L762-L766, May 1998

Effect of anion secretion inhibitors on mucin content of airway submucosal gland ducts

Sarah K. Inglis, Michel R. Corboz, and Stephen T. Ballard

Department of Physiology, College of Medicine, University of South Alabama, Mobile, Alabama 36688

In porcine bronchi, inhibition of both Cl- and HCO-3 transport is required to block the anion secretion response to ACh and to cause mucus accumulation within ACh-treated submucosal gland ducts [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]. In this previous study, a combination of three potential HCO-3 transport inhibitors [1 mM acetazolamide, 1 mM DIDS, and 0.1 mM dimethylamiloride (DMA)] was used to block carbonic anhydrase, Cl-/HCO-3 exchange, and Na+/H+ exchange, respectively. The aim of the present study was to obtain a better understanding of the mechanism of ACh-induced HCO-3 secretion in airway glands by determining which of the three inhibitors, in combination with bumetanide, is required to block anion secretion and so cause ductal mucin accumulation. Gland duct mucin content was measured in distal bronchi isolated from domestic pigs. Addition of either bumetanide alone, bumetanide plus acetazolamide, or bumetanide plus DIDS had no significant effect on ACh-induced mean gland duct mucin content. In contrast, glands treated with bumetanide plus DMA as well as glands treated with all four anion transport blockers were almost completely occluded with mucin after the addition of ACh. These data suggest that mucin is cleared from the ducts of bronchial submucosal glands by liquid generated from Cl-- and DMA-sensitive HCO-3 transport.

acetylcholine; airway epithelium; bicarbonate secretion; bronchi; cystic fibrosis; mucus


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