Effect of aldosterone on ion transport by rabbit colon in vitro.

Segments of descending colon obtained from rabbits, that had been maintained on drinking water containing 25 mM NaCl and an artificial diet which contains 1% Na and is nominally K-free, respond to aldosterone in vitro (after a 30 to 60-min lag period) with a marked increase in the short-circuit current (Isc), an equivalent increase in the rate of active Na absorption (JNa net) and a decline in tissue resistance (Rt). Aldosterone also brings about a marked increase in the unidirection influx of Na into the cells across the mucosal membrane ("zero-time" rate of uptake) which does not differ significantly from the inrease m Isc. Treatment of control tissues with amphotericin B brings about sustained increases in Isc and JNa net to levels observed in aldosterone-treated tissues. However, addition of amphotericin B to the mucosal solution of aldosterone-treated tissues does not result in a sustained increase in Isc or JNa net and these values do not differ markedly from those observed in control tissues treated with amphotericin B. These findings, together with other evidence that Na entry in the presence of amphotericin B is sufficiently rapid to saturate the active Na extrusion mechanism at the baso-lateral membrane, are consistent with the notion that the aldosterone-induced protein increases the permeability of the mucosal membrane to Na but does not increase the "saturation level" of the active Na "pump" within the time-frame of these studies (3 hr). Finally, aldosterone has no effect on the bidirectional or net transepithelial movements of K under short-circuit conditions, suggesting that the enhanced secretion of K observed in vivo is the result of increased diffusion of K from plasma to lumen via paracellular pathways in response to an increased transepithelial electrical potential difference (lumen negative).