Effect of mineralocorticoids on collecting duct hydrogen ion secretion in the rabbit

Robson, Wm. Lane M.; Halperin, Mitchell L.; Stinebaugh, Bobby J.; Goldstein, M. B.

doi:10.1139/y81-037

Cited by 3 publications

(2 citation statements)

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“…Third, urinary Pco2, even in sham controls receiving bicarbonate, was much lower in the previous study (53 mmHg) than that routinely observed in bicarbonate loaded control rats in our laboratory (100-120 mmHg) (14) (27). Compatible with our data, however, Robson et al (37) have reported that mineralocorticoid (9-afluorohydrocortisone) administration to adrenal intact rabbits increased the U-B Pco2 relative to controls undergoing a similar bicarbonate diuresis.…”

Section: Effects Ofcmasupporting

confidence: 63%

Effect of selective aldosterone deficiency on acidification in nephron segments of the rat inner medulla.

DuBose

Caflisch²

1988

J. Clin. Invest.

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Mineralocorticoid plays a role in urinary acidification and acid-base balance, but the response of the inner medulla to aldosterone has not been elucidated. A model of selective aldosterone deficiency (SAD) with hyperkalemia and hyperchloremic metabolic acidosis was employed to assess segmental acidification by measuring in situ pH, titratable acidity (TA) and total ammonia (Am). Hydrogen ion secretion was also examined as a function of the increment in in situ Pco2 in the collecting duct during bicarbonate loading. SAD rats were compared to ADX controls that received adrenalectomy and chronic replacement of gluco-and mineralocorticoid and to rats with chronic metabolic acidosis induced by oral NH4Cl (CMA). Both fractional and absolute delivery of Am to the loop of Henle was lower in SAD vs. CMA rats (1.34 to 3.63 mM, P < 0.01). Delivery of Am to the base and tip collecting duct (BCD and TCD) was also markedly lower in SAD (1.50 vs. 0.52 and 1.77 vs. 0.47 mM, respectively, P < 0.01). Net addition of Am and net acid between BCD and TCD, observed in CMA rats, was not observed in SAD despite equivalent degrees of systemic metabolic acidosis. Similarly, the concentration gradient favoring transfer of NH3 between loop of Henle and CD was reduced in SAD. During bicarbonate loading the increment in Pco2 at BCD, TCD and in final urine was significantly lower in SAD rats than in adrenal intact bicarbonate-loaded rats. Therefore, the acidification defect in this model of SAD appears to be a result of a decrease in ammonia production and delivery to the loop of Henle, impaired transfer from loop to collecting duct and reduction in the rate of H+ secretion by the collecting duct.

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Section: Effects Ofcmasupporting

confidence: 63%

Effect of selective aldosterone deficiency on acidification in nephron segments of the rat inner medulla.

DuBose

Caflisch²

1988

J. Clin. Invest.

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“…dog, and rat and has been interpreted as evidence of a deficit in distal (collecting duct) acidification in this herbivorous spe cies. Slightly or moderately increased (U-B)pC02 values have been measured in the alkaline urine of rabbits with 'normalized' serum levels of potassium [1], after oral a-9-fluorohydrocortisone [4] and after intrave nous furosemide [5]. Recently, Cruz-Soto et al [3] reported an increase in (U-B)pC02 in nonacidotic rabbits infused simultaneously with bicarbonate and acetazolamide.…”

Section: Introductionmentioning

confidence: 99%

Effect of Carbonic Anhydrase Inhibition on (U-B)pCO<sub>2</sub> in the Alkaline Urine of the Rabbit

Kekomäki¹,

Maren²,

Wingo

1986

Kidney Blood Press Res

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We studied factors influencing urine pCO₂minus blood pCO₂ [(U-B)pCO₂] in rabbits infused with sodium bicarbonate solutions. Unlike other species, the rabbit does not develop a significant (U-B)pCO₂ (urine pCO₂ > blood pCO₂) after alkali or acid buffer infusion. However, intravenous acetazolamide immediately induced a significant (U-B)pCO₂· The effect could not be related to the blood pH or pCO₂ the urinary concentration of bicarbonate or inorganic phosphate, or to changes in plasma potassium concentration. Methazolamide was also effective in increasing (U-B)pCO₂- This significant (U-B)pCO₂ was present after carbonic anhydrase inhibition in rabbits subjected to chronic partial obstruction of urinary flow and in rabbits treated with 11-desoxycorticosterone acetate (DOCA). We propose that carbon dioxide is normally dissipated from the alkaline urine of the rabbit by a distal tubular mechanism, which involves catalytic conversion of carbon dioxide to bicarbonate. Inhibition of carbonic anhydrase leads to the formation of a significant (U-B)pCO₂· In the rabbit, pCO₂ may be an index of collecting duct acidification under certain circumstances; however, the relation of collecting duct acidification to the high (U-B)pCO₂ during the inhibition of carbonic anhydrase remains to be determined.

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H+ transport by the aldosterone-deficient rat distal nephron

Kornandakieti

Tannen

1984

Kidney International

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The effect of aldosterone on distal nephron acidification was investigated by comparing isolated perfused kidneys from adrenalectomized rats treated for 3 to 5 days with dexamethasone alone (10 micrograms/day i.p.) and from rats given in addition a physiologic dose of d-aldosterone (10 micrograms/day in oil s.c.). The maximal pH gradient between urine and perfusate, determined at a perfusate pH of 6.7 with glucose as the sole substrate, did not differ significantly between the aldosterone deplete and replete groups (1.27 +/- 0.12 vs. 1.35 +/- 0.12). H+ secretory capacity of the distal nephron was determined by perfusing kidneys at pH 6.8 and providing saturating quantities of urinary buffer in the form of creatinine. Under these experimental conditions kidneys from aldosterone deplete rats had a higher urine pH and lower excretion rate of titratable acid indicative of a defect in H+ secretion. Acid secretion below a pH of 6.0 (T.A.-pH 6.0), an index of H+ secretion by the distal nephron, was also significantly lower in the aldosterone deplete kidneys. Thus, aldosterone depletion decreased the H+ secretory capacity of the distal nephron, but had no clear effect on the force of the pump as reflected by the maximal pH gradient. Amiloride (10(-5) M) was added to the perfusate of kidneys undergoing the H+ secretory capacity protocol to distinguish between sodium-linked and sodium-independent effects of aldosterone. The difference in T.A. pH 6.0 between aldosterone deplete and replete kidneys was reduced by approximately 70% in the presence of amiloride. This indicates that a substantial portion of the aldosterone-dependent component of distal nephron H+ secretion is mediated by a sodium-dependent mechanism.

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Effect of mineralocorticoids on collecting duct hydrogen ion secretion in the rabbit

Cited by 3 publications

References 0 publications

Effect of selective aldosterone deficiency on acidification in nephron segments of the rat inner medulla.

Effect of selective aldosterone deficiency on acidification in nephron segments of the rat inner medulla.

Effect of Carbonic Anhydrase Inhibition on (U-B)pCO<sub>2</sub> in the Alkaline Urine of the Rabbit

H+ transport by the aldosterone-deficient rat distal nephron

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