Aldosterone stimulation of acidification of urine by isolated urinary bladder of the Colombian toad

Ludens, JH; Fanestil, Darrell D.

doi:10.1152/ajplegacy.1974.226.6.1321

Cited by 53 publications

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“…Aldosterone enhances renal acid excretion and thus has an important role in the regulation of acid-base homeostasis (1,2). The possibility that changes in extracellular fluid pH affect the adrenal production or release of aldosterone has not been systematically evaluated.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Acute Metabolic Acidosis on Plasma Cortisol, Renin Activity and Aldosterone

et al. 1979

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The effect of metabolic acidosis on the renin-aldosterone system remains unclear. In the present study anesthetized mongrel dogs (n = 19) were infused at similar rates with 0.45% NaCl (controls), HCl or NH₄Cl (2.5mEq/kg) for 1-3 h. The induced metabolic acidosis in the two experimental groups was not associated with increases in plasma renin activity. Plasma cortisol (as a marker for ACTH secretion) and serum potassium concentration increased in both HCl- and NH₄Cl-treated animals. Plasma aldosterone increased after 30 min in the HCl group and 60 min in the NH₄C1 group and did not change in controls. These findings demonstrate that metabolic acidosis induced by HCl or NH₄Cl is associated with increased aldosterone production without concomitant changes in plasma renin activity.

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Section: Discussionmentioning

confidence: 99%

The Effect of Acute Metabolic Acidosis on Plasma Cortisol, Renin Activity and Aldosterone

et al. 1979

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“…Observations such as those cited above, coupled with the demonstration that urinary acidification in anuran bladders proceeds by a mechanism that is molecularly independent of sodium yet stimulated by aldosterone (10) and dexamethasone (11), raise the possibility that a sodium-independent steroid responsive acidifying segment (or segments) exists in the mammalian kidney.…”

Section: Introductionmentioning

confidence: 97%

Mineralocorticoid modulation of rabbit medullary collecting duct acidification. A sodium-independent effect.

Seldin²,

et al. 1983

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A B S T R A C T Rabbit medullary collecting duct (MCD) from inner stripe of outer medulla has been identified as a major distal nephron acidification site. The isolated, perfused tubule technique was used to examine the roles of mineralocorticoid and glucocorticoid in regulation of MCD acidification. Surgical adrenalectomy reduced bicarbonate reabsorptive rate (JHCO3, pmol * mm-'l min-') from the normal of 9.79±1.21 to 0.67±1.1. Chronic administration of deoxycorticosterone acetate (DOCA) increased JHCO3 of MCD significantly to 18.02±1.62 whereas chronic dexamethasone administration did not affect JHCO3. The direct effects of aldosterone and dexamethasone upon MCD acidification were examined by perfusing tubules harvested from adrenalectomized rabbits in the presence of aldosterone or dexamethasone. Aldosterone, at 5 X 10-8 M, increased JHCO3 significantly from 1.27±0.28 to 3.09±0.34. At 10-6 M, aldosterone produced a greater increase in JHCO3 from 0.67±1.1 to 9.39±1.59. In vitro dexamethasone treatment had no effect on JHCO3. Studies examining the sodium dependence of aldosterone-stimulated acidification demonstrated that JHCO3 in tubules harvested from normal and deoxycorticosterone acetate-treated animals was unaffected by total replacement of sodium with tetramethylammonium. Likewise, luminal amiloride (5 X 10-5 M) had no effect on JHCO3 in tubules har-

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“…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.…”

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confidence: 99%

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

Al‐Awqati¹,

Norby²,

Mueller³

et al. 1976

J. Clin. Invest.

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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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Aldosterone stimulation of acidification of urine by isolated urinary bladder of the Colombian toad

Cited by 53 publications

References 0 publications

The Effect of Acute Metabolic Acidosis on Plasma Cortisol, Renin Activity and Aldosterone

The Effect of Acute Metabolic Acidosis on Plasma Cortisol, Renin Activity and Aldosterone

Mineralocorticoid modulation of rabbit medullary collecting duct acidification. A sodium-independent effect.

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

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