Abstract
The reversible inhibition of transepithelial sodium transport achieved with amiloride (and triamterene) was evaluated in amphibian preparations stimulated with aldosterone so as to provide further information regarding a possible influence of this hormone on the apical border of target cells. When aldosterone secretion was enhanced by withdrawal of sodium from toad (Bufo marinus) habitat, sensitivity of abdominal skin to amiloride decreased; the same occurred in skin and bladder preparations incubated with aldosterone for several hours. Amiloride proved a less efficient blocker of sodium transport by toad skin exposed to vasopressin and to ouabain; both substances are capable or raising cell sodium content. It is therefore proposed that the decrease in sensitivity to amiloride of amphibian epithelia treated with aldosterone results from an increase in target cell sodium, itself due to a hormone-induced increase in sodium conductance at the apical cell border. Glucose, which enhanced markedly the rate of sodium transport in preparations treated with aldosterone for several hours, failed to decrease any further the response to amiloride; this is taken as an argument for an additional (? secondary) influence of aldosterone on the cell's metabolic machinery connected with the operation of the sodium ‘pump’.