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1 Tayside Institute of Child Health, University of Dundee, Dundee, Tayside, United Kingdom
* To whom correspondence should be addressed. E-mail: s.k.inglis{at}dundee.ac.uk.
Secretion of HCO3- by airway submucosal glands is essential for normal liquid and mucus secretion. Since the liquid bathing the airway surface (ASL) is acidic, it has been proposed that the surface epithelium may acidify HCO3--rich glandular fluid. The aim of this study was to investigate the mechanisms by which intact distal bronchi, that contain both surface and glandular epithelium, modify pH of luminal fluid. Distal bronchi were isolated from pig lungs, cannulated in a bath containing HCO3- buffered solution and perfused continually with an aliquot of similar, lightly buffered solution (LBS) in which NaCl replaced NaHCO3- (pH7 with NaOH). The pH of this circulating LBS initially acidified (by 0.053±0.0053pHunits) and transepithelial PD depolarised. The magnitude of acidification was increased when pHLBS was higher. This acidification was unaffected by luminal DMA (100µM), but was inhibited by 100nM bafilomycin A1 (by 76±13%), suggesting involvement of v-H+ ATPase. Addition of ACh (10µM) evoked alkalinisation of luminal LBS and hyperpolarisation of transepithelial PD. The alkalinisation was inhibited in HCO3- -free solutions containing acetazolamide (1mM) and by DMA, and enhanced by bumetanide (100µM), an inhibitor of Cl- secretion. The hyperpolarisation was unaffected by these manoeuvres. The anion channel blocker NPPB (300µM), and combined treatment with DMA and bumetanide blocked both the alkalinisation and hyperpolarisation responses to ACh. These results are consistent with earlier studies showing that ACh evokes glandular secretion of HCO3- and Cl-. Isolated distal airways thus secrete both acid and base equivalents.
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