Mechanism of ion transport by avian salt gland primary cell cultures

Confluent sheets formed from primary culture of avian salt gland secretory cells exhibit a short-circuit current (I(sc)) in response to cholinergic and β-adrenergic stimulation [Lowy, R.J., D.C Dawson, and S.A. Ernst. Am J. Physiol. 249 (Cell Physiol. 18): C41-C47, 1985]. To establish the ionic basis for the I(sc) transmural fluxes of ²²Na and ³⁶Cl were measured. Under short-circuit conditions there was little net flux of either iron in the absence of agonists. Addition of carbachol elevated net serosal-to-mucosal Cl flux to 1.71 μeq·h^-1·cm^-2, whereas a smaller increase to 0.85 μeq·h^-1·cm^-2 occurred with isoproterenol. Neither agonist altered net Na flux. The stimulated I(sc) accounted for 70% of the net Cl flux induced by carbachol and nearly 100% of that induced by isoproterenol. Replacement of Cl by gluconate or Na by choline abolished (carbachol) or greatly reduced (isoproterenol) the I(sc), which could be restored in a dose-dependent fashion by ion restitution. Active ion transport was preferentially inhibited by basal (vs. apical) addition of ouabain, furosemide, or barium. The results provide evidence that cholinergic and β-adrenergic agonists elicit active transmural Cl secretion. They further suggest that transport is dependent on the Na⁺-K⁺-adenosine-triphosphatase, a Na-Cl contransport process, and a basal K conductance, all features of a secondary active Cl secretory mechanism.