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and
HCO3 transport
1 Department of Physiology, College of Medicine, University of South Alabama, Mobile, Alabama 36688; and 2 Department of Pharmacology, School of Medicine, University of North Carolina, Chapel Hill, North Carolina 27599
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. Mol. Physiol. 16): L372-L377, 1997]. The present study quantified contributions
of Cl and
HCO3 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 · cm2 · h1.
Bumetanide (10 µM) pretreatment reduced acetylcholine-induced liquid
and Cl secretion rates by
~70%, but HCO3 secretion fell by
only 40%. Dimethylamiloride (DMA; 100 µM) pretreatment reduced
Cl secretion rates by ~15%, but
HCO3 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
HCO3 secretion. We speculate that the
principal source of this liquid is submucosal glands. Crossover
inhibition of bumetanide on HCO3 secretion and DMA on Cl
secretion implies modulation of anion secretion secondary to changes in
cell electrolyte composition.
cystic fibrosis; dimethylamiloride; bumetanide; bronchi; submucosal glands; bicarbonate; chloride
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