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Extracellular sodium is required for methacholine‐induced secretion of mucus glycoconjugates from canine tracheal explants
Author(s) -
Barsigian Carl,
Barbieri Edward J.
Publication year - 1990
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.290080308
Subject(s) - mucus , secretion , veratridine , dids , extracellular , endocrinology , medicine , methacholine , amiloride , sodium , chemistry , intracellular , biology , biochemistry , sodium channel , ecology , respiratory disease , organic chemistry , lung , membrane
Extracellular sodium is known to influence secretion by certain secretory cells, possibly by mobilizing calcium from cellular stores or by altering intracellular pH via regulation of a Na + ‐H + antiport system. Using canine tracheal explants, we determined whether agents which alter sodium fluxes are capable of modulating basal or cholinergically‐induced secretion of mucus glycoconjugates. Methacholine, a cholinergic agonist, increased mucus secretion from explants incubated in the presence or absence of calcium, but had no effect on secretion when incubated in sodium‐deficient media, indicating (a) that cholinergically‐induced secretion can be mediated by mobilization of cellular calcium and (b) that extracellular sodium was required for this stimulatory effect. Several agents which increase intracellular sodium were tested for their effect on mucus secretion. Ouabain, a sodium pump inhibitor, and veratridine, a sodium channel activator, did not significantly affect control or methacholine‐induced secretion; gramicidin, a sodium ionophore, also had no effect on basal release. Tetrodotoxin, a sodium channel inhibitor, was also without effect on basal or methacholine‐stimulated mucus release. Agents which alter intracellular pH were also examined for their effects on basal or methacholine‐induced glycoconjugate secretion. Amiloride, which decreases intracellular pH by inhibiting Na + ‐H + exchange, produced a 19 per cent increase in basal secretion (not statistically significant), but had no effect on methacholine‐induced secretion. An agent, 4,4′‐diisothiocyanostilbene‐2,2′‐disulfonic acid (DIDS), which decreases intracellular pH by inhibiting HCO 3 − −Cl − exchange, elicited decreases in both basal and methacholine‐induced secretion, but the inhibition did not reach statistical significance. Thus extracellular sodium is required for cholinergically‐induced glycoconjugate secretion from canine tracheal explants and the underlying mechanism does not involve sodium influx into the cell, but may possibly be mediated by alterations in intracellular pH.