Catecholamine-induced changes in ion transport in short-circuited frog skin and the effect of beta-blockade

1. A method for measuring bidirectional Cl fluxes has been used to estimate net Cl movements in short-circuited frog skin and to compare these with the short-circuit current (Isc) and Na fluxes. 2. In some experiments bidirectional fluxes of both Na and Cl were measured simultaneously. It was found that the algebraic sum of the net fluxes of these two ions did not differ significantly from the values of Isc, either in untreated or catecholamine-treated skins, except for the half-hour period immediately after catecholamine addition. 3. The net effluxes of Cl produced by noradrenaline (1-6 X 10(-5)M), isoprenaline (8 X 10(-7)M) and adrenaline (6 and 15 X 10(-6)M) were of similar magnitude for each catecholamine. The magnitude of the Cl response measured as a flux ratio was related to a certain extent to the precatecholamine Cl conductance. 4. The net Na influx was increased by isoprenaline and reduced by noradrenaline. 5. Addition of the beta-adrenergic blocking agent oxprenolol (4-5 X 10(-5)M) to skins stimulated by catecholamine resulted in the disappearance of the net Cl movement and fall in skin conductance and Isc. This fall was similar in magnitude to, and correlated with the mean rise in Isc produced by isoprenaline, but of significantly greater magnitude in the case of noradrenaline. 6. The changes in Na influx were strongly associated with the changes in Isc following catecholamine addition. Similarly, the changes in Na efflux and Cl efflux were correlated, suggesting the Na fluxes to be dissociated, influx and efflux changes perhaps taking place at different loci. 7. Acetazolamide (1-2 X 10(-4)M), added either before or during the noradrenaline stimulation, had no effect on the Cl efflux response. 8. The tissue exchange of Cl from the outside bathing medium after 4 hr was greater in catecholamine-stimulated skins than in those in which the response had been blocked by oxprenolol. 9. These findings were taken to support a model entailing a neutral NaCl pump resident in the mucous glands and an epithelial Na pump enhanced by beta- and inhibited by alpha-adrenergic stimulation.