A B S T R A C T Aldosterone stimulates not only Na4 absorption but also urinary acidification. In this investigation the effects of aldosterone on H4 transport are examined in vitro in turtle bladder, a urinary membrane in which several of the factors controlling H4 transport have been defined. H+ transport was increased in bladder halves exposed to aldosterone compared to control halves. Stimulation of H4 secretion was observed as early as 1 h after addition of aldosterone and occurred before that of Na4 transport. In bladders depleted of endogenous substrate addition of glucose increased H+ transport more in aldosterone-treated halves (10.0±1.3 nmol/min) than in control halves (6.8±2.3). Addition of pyruvate failed to increase H+ transport (-0.3+0.7) in control halves but caused significant increments (2.4±0.5) in aldosterone-treated halves. In aldosteronetreated bladders glucose caused larger increments (16.5 ±2.7) in H+ transport than pyruvate (9.3±2.0) when halves of the same bladders were compared. Na+ transport, however, was equally increased by the two substrates. Despite the differences in time course and substrate requirements between the stimulation of H+ and Na+ transport, both increases were abolished by actinomycin-D.To examine the effect of aldosterone on the force of the H+ pump, protonmotive force, the pH gradient that would nullify the transport rate was determined with and without aldosterone. Aldosterone did not alter protonmotive force but significantly increased the slope of the H+ transport rate on the applied pH gradient. It is concluded that aldosterone stimulates H4 transport independently of Na+ transport. It increases the responsiveness of the transport rate to glucose and to a lesser extent pyruvate, an effect probably secondary to the increased transport rate. Equivalent circuit analysis indicates that aldosterone facilitates the flow of protons through the active transport pathway but does not increase the force of the pump. INTRODUCTION Several lines of evidence indicate that aldosterone not only stimulates the renal absorption of sodium but also the process of urinary acidification. To which extent the increased acidification is a function of accelerated sodium absorption remains to be determined. At least some studies suggest that acidification may be stimulated independently of sodium transport. Lifschitz et al.(1) provided some evidence in the dog that renal H4 secretion is stimulated by a pathway that does not involve DNA-dependent synthesis of RNA. Ludens and Fanestil (2) reported that aldosterone increased the rate of acidification in the urinary bladder of the Colombian toad, as judged from the reversed short-circuit current after inhibition of sodium transport; they did not attempt, however, to explore the transport step in acidification that was stimulated by the hormone.Since turtle urinary bladder responds to aldosterone (3) and is capable of urinary acidification under conditions that permit close examination of the transport components (4), this preparation was se...

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