Differential effects of acute mineralo- and glucocorticosteroid administration on renal acid elimination

Wilcox, Christopher S.; Cemerikic, Dusan; Giebisch, Gerhard

doi:10.1038/ki.1982.61

Cited by 53 publications

(38 citation statements)

References 31 publications

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“…Several reports have documented the importance of glucocorticoids in the renal response to metabolic acidosis. In ADX rats, there is impaired renal glutamine uptake and ammoniagenesis in response to acidosis (47), and increasing doses of glucocorticoids raise ammonia excretion (48). We have extended the report (12) that acidosis raises plasma corticosterone by showing that corticosterone production, as reflected in its 24-h urinary excretion, is stimulated by acidosis (Fig.…”

Section: Discussionmentioning

confidence: 54%

Metabolic acidosis stimulates protein degradation in rat muscle by a glucocorticoid-dependent mechanism.

May¹,

Kelly²,

Mitch³

1986

J. Clin. Invest.

348

221

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Metabolic acidosis is associated with enhanced renal ammoniagenesis which is regulated, in part, by glucocorticoids. The interaction between glucocorticoids and chronic metabolic acidosis on nitrogen utilization and muscle protein metabolism is unknown. In rats pair-fed by gavage, we found that chronic acidosis stunted growth and caused a 43% increase in urinary nitrogen and an 87% increase in urinary corticosterone. Net protein degradation in incubated epitrochlearis muscles from chronically acidotic rats was stimulated at all concentrations of insulin from o to 104 MU/ml. This effect of acidosis persisted despite supplementation of the media with amino acids with or without insulin, indomethacin, and inhibitors of lysosomal thiol cathepsins. Acidosis did not change protein synthesis; hence, the increase in net protein degradation was caused by stimulation of proteolysis. Acidosis did not increase glutamine production in muscle. The protein catabolic effect of acidosis required glucocorticoids; protein degradation was stimulated in muscle of acidotic, adrenalectomized rats only if they were treated with dexamethasone. Moreover, when nonacidotic animals were given 3 isg/100 g of body weight dexamethasone twice a day, muscle protein degradation was increased if the muscles were simply incubated in acidified media. We conclude that chronic metabolic acidosis depresses nitrogen utilization and increases glucocorticoid production. The combination of increased glucocorticoids and acidosis stimulates muscle proteolysis but does not affect protein synthesis. These changes in muscle protein metabolism may play a role in the defense against acidosis by providing amino acid nitrogen to support the glutamine production necessary for renal ammoniagenesis.

show abstract

Section: Discussionmentioning

confidence: 54%

Metabolic acidosis stimulates protein degradation in rat muscle by a glucocorticoid-dependent mechanism.

May¹,

Kelly²,

Mitch³

1986

J. Clin. Invest.

348

221

View full text Add to dashboard Cite

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“…These effects are exerted largely on such distal nephron segments as the cortical and medullary collecting ducts. 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).…”

Section: Discussionmentioning

confidence: 89%

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

Winter

Schulz

Giebisch

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

115

100

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“…Although aldosterone is known to stimulate proton secretion in collecting ducts (reviewed in reference 28), to what extent the acidosis-induced increment in the circulating aldosterone level contributes to the renal response against acidosis remains to be established. The presence of circulating glucocorticosteroids has been shown to be necessary for a normal adaptive increase in renal ammonia and phosphate excretion in response to acute and chronic metabolic acidosis in the rat (17,(29)(30)(31)(32). Results in the present study also support the hypothesis of a role for adrenal hormones in the renal response to acute metabolic acidosis inasmuch as absolute values of urinary excretion rates of phosphate, ammonium, and thus net acid were lower in ADX than in intact rats during both control and acidosis periods.…”

Section: Discussionmentioning

confidence: 99%

Acute metabolic acidosis enhances circulating parathyroid hormone, which contributes to the renal response against acidosis in the rat.

Bichara¹,

Mercier²,

Borensztein³

et al. 1990

J. Clin. Invest.

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Acute PTH administration enhances final urine acidification in the rat. HCl was infused during 3 h in rats to determine the parathyroid and renal responses to acute metabolic acidosis. Serum immunoreactive PTH (iPTH) concentration significantly increased and nephrogenous adenosine 3',5'-cyclic monophosphate tended to increase during HCO loading in intact and adrenalectomized (ADX) rats despite significant increments in plasma ionized calcium. Strong linear relationships existed between serum iPTH concentration and arterial bicarbonate or proton concentration (P < 0.0001). Serum iPTH concentration and NcAMP remained stable in intact time-control rats and decreased in CaCl2-infused, nonacidotic animals. Urinary acidification was markedly reduced in parathyroidectomized (PTX) as compared with intact rats during both basal and acidosis states; human PTH-(1-34) infusion in PTX rats restored in a dose-dependent manner the ability of the kidney to acidify the urine and excrete net acid. Acidosis-induced increase in urinary net acid excretion was observed in intact, PTX, and ADX, but not in ADX-thyroparathyroidectomized rats.We conclude that (a) acute metabolic acidosis enhances circulating PTH activity, and (b) PTH markedly contributes to the renal response against acute metabolic acidosis by enhancing urinary acidification. (J. Clin. Invest. 1990. 86:430-443.)

show abstract

Differential effects of acute mineralo- and glucocorticosteroid administration on renal acid elimination

Cited by 53 publications

References 31 publications

Metabolic acidosis stimulates protein degradation in rat muscle by a glucocorticoid-dependent mechanism.

Metabolic acidosis stimulates protein degradation in rat muscle by a glucocorticoid-dependent mechanism.

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

Acute metabolic acidosis enhances circulating parathyroid hormone, which contributes to the renal response against acidosis in the rat.

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Differential effects of acute mineralo- and glucocorticosteroid administration on renal acid elimination

Cited by 53 publications

References 31 publications

Metabolic acidosis stimulates protein degradation in rat muscle by a glucocorticoid-dependent mechanism.

Metabolic acidosis stimulates protein degradation in rat muscle by a glucocorticoid-dependent mechanism.

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

Acute metabolic acidosis enhances circulating parathyroid hormone, which contributes to the renal response against acidosis in the rat.

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