Dual action of aldosterone on toad bladder: Na+ permeability and Na+ pump modulation.
The effects of aldosterone on the functional characteristics of the Na+ entry step across the apical membrane and on the Na+ exit step across the basolateral membrane of the urinary bladder of toads were examined using amiloride and ouabain as probes of the respective surfaces of the cell. Aldosterone stimulated Na+ transport with a concurrent increase in the transepithelial electrical conductance as did two other agents, vasopressin (ADH) and p-chloromercuriphenylsulfonate (PCMPS), primarily active on the apical membrane. Unlike the effects of ADH and PCMPS, however, the effect of aldosterone on Na+ conductance was blocked by actinomycin D and was associated with a decreased sensitivity of the apical Na+ channel to amiloride. In addition, aldosterone increased the sensitivity of the Na+ pump on the basolateral side to ouabain, an effect that was dependent on the metabolic state of the urinary bladder. These results support the inference of coordinate effects on Na+ permeability of the apical membrane and the Na+ pump of the basolateral membrane. Both effects of aldosterone appear to be dependent on the metabolic state of the transporting epithelium.
D000450:Aldosterone / Q000494:pharmacology*; D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D002024:Bufo marinus; D002729:Chloromercuribenzoates / Q000494:pharmacology; D003609:Dactinomycin / Q000494:pharmacology; D007473:Ion Channels / Q000187:drug effects; D010042:Ouabain / Q000494:pharmacology; D010539:Permeability; D012964:Sodium / Q000378:metabolism*; D001743:Urinary Bladder / Q000187:drug effects*; D014667:Vasopressins / Q000494:pharmacology; D020245:p-Chloromercuribenzoic Acid
D002729:Chloromercuribenzoates; D007473:Ion Channels; D014667:Vasopressins; D003609:Dactinomycin; D000450:Aldosterone; D020245:p-Chloromercuribenzoic Acid; D010042:Ouabain; D000584:Amiloride; D012964:Sodium