Abstract
Vasoactive intestinal peptide (VIP) normally induces liquid secretion by tracheobronchial submucosal glands, but this function is lost in cystic fibrosis (CF) airways suggesting that this process critically depends on CFTR anion channels (Joo et al. J Biol Chem 277:50710–50715, 2002). The present study was undertaken to document the ionic mechanism of VIP-induced liquid secretion which is not well-understood. Intact bronchi were dissected from the lungs of young pigs and cannulated. When stimulated with VIP, bronchi secreted 7.34±μL·cm−2·h−1. Removal of Cl− from the bath solution caused the rate of secretion to fall to 28.6±5.6% of control. Removal of both Cl− and HCO3− reduced secretion rate to 13.6±3.4% of control. Bumetanide, an NKCC inhibitor, reduced secretion to 45.6±9.6% of control. The anion channel blockers NPPB, DPC, and glibenclamide reduced VIP-induced secretion to 3.9±1.6%, 14.7±4.5%, and 26.7±7.7% of control, respectively. Removal of the airway surface epithelium did not affect the baseline VIP secretion response nor its inhibition by NPPB. We conclude that the liquid secretion response of porcine bronchi originates from submucosal glands, is driven by a combination of HCO3− secretion and bumetanide-sensitive Cl− secretion, and is likely mediated by CFTR. Supported by NIH HL63302
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