Characteristics of stimulation of H+ transport by aldosterone in turtle urinary bladder.

Abstract

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...

Nongenomic stimulation of vacuolar H + -ATPases in intercalated renal tubule cells by aldosterone

“…Whereas adrenalectomy interferes with net acid excretion, aldosterone has been shown to correct the inability to establish steep urine-to-blood pH gradients (31). Furthermore, aldosterone increases the activity of vacuolar H ϩ -ATPases in rat and rabbit cortical and medullary collecting ducts, and these effects are mimicked in isolated turtle bladder (32). Evidence that this mineralocorticoid is necessary for appropriate urinary acidification is also derived from patients with inborn or acquired aldosterone deficiency syndromes (distal renal tubular acidosis type IV) or in animal models with adrenalectomy or pharmacological blockade of the aldosterone pathway (10,(33)(34)(35)(36).…”

SDF1 induction by acidosis from principal cells regulates intercalated cell subtype distribution

“…In the collecting tubule, as in the other acidifying segment (the proximal tubule), there are acute and chronic responses to an acid load. Acute responses might include the following: exocytosis of vesicles containing H + ATPases, thereby increasing the number of proton pumps on the surface (1, 2); assembly and disassembly of various subunits; and kinetic effects on the ATPase mediated by cytoplasmic acidification, kinetic activation of soluble adenyl cyclase (3), as well as by hormones such as angiotensin II (4) and aldosterone (5).…”

Spironolactone. An aldosterone agonist in the stimulation of H+ secretion by turtle urinary bladder.

“…was added in 50 ,l of methanol to give a final concentration of 0.5 ,uM. This concentration is half the concentration used by LeFevre (16) in the turtle bladder and has been effective in the stimulation of JH and JNa in our previous study (14). Spironolactone (Sigma Chemical Co.), 17-hydroxy-7a-mercapto-3-oxo-17a-pregn-4-ene-21-carboxylic acid y-lactone 7-acetate, was added to 50 ,ul of methanol to give a final concentration of 50 ,u M. The same volume of methanol was added to the control halves.…”

“…Alternatively, aldosterone might stimulate these secretory processes by separate mechanisms. Recent studies have shown that aldosterone can directly stimulate hydrogen secretion in two urinary epithelia; in the bladder ofthe Colombian toad (13) and the bladder of the freshwater turtle, Pseudemys scripta (14). The studies in turtle urinary bladder have further shown that the stimulation of hydrogen secretion precedes that of sodium transport and has different substrate requirements (14).…”