Glucocorticoid and Acid-Base Homeostasis: Effects on Glutamine Metabolism and Transport

Welbourne, T. C.

doi:10.1016/s0272-6386(89)80206-9

Cited by 8 publications

(2 citation statements)

References 12 publications

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“…Increased bone buffering capacity [17,[58][59][60][61][62] Increased levels in secondary hyperparathyroidism [63] Association of secondary hyperparathyroidism with worsening CKD, but causal relationship is unclear [63,64] Glucocorticoids Increased levels [65] Increased glutamine delivery and kidney ammonia production. increased proximal tubule acid secretion [66][67][68][69] Higher levels of glucocorticoids in CKD are not associated with enhanced glutamine delivery. Unclear whether there is resistance to action [70] Association of high glucocorticoids with progression but unclear whether the high glucocorticoid levels cause worsening of CKD [71,72] Table 1.…”

Section: Aldosteronementioning

confidence: 99%

“…Dexamethasone supplementation increases the apical membrane activity of the NHE-3 isoform of the Na + -H + exchanger in brush border membranes [68]. Glucocorticoids are also important in enhancing the uptake and oxidation of glutamine, the major substrate for ammoniagenesis, by the proximal tubules [69]. The effects of glucocorticoids on distal acidification are less clear.…”

Section: Glucocorticoidsmentioning

confidence: 99%

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The Role of the Endocrine System in the Regulation of Acid–Base Balance by the Kidney and the Progression of Chronic Kidney Disease

Nagami,

Kraut

2024

IJMS

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Systemic acid–base status is primarily determined by the interplay of net acid production (NEAP) arising from metabolism of ingested food stuffs, buffering of NEAP in tissues, generation of bicarbonate by the kidney, and capture of any bicarbonate filtered by the kidney. In chronic kidney disease (CKD), acid retention may occur when dietary acid production is not balanced by bicarbonate generation by the diseased kidney. Hormones including aldosterone, angiotensin II, endothelin, PTH, glucocorticoids, insulin, thyroid hormone, and growth hormone can affect acid–base balance in different ways. The levels of some hormones such as aldosterone, angiotensin II and endothelin are increased with acid accumulation and contribute to an adaptive increase in renal acid excretion and bicarbonate generation. However, the persistent elevated levels of these hormones can damage the kidney and accelerate progression of CKD. Measures to slow the progression of CKD have included administration of medications which inhibit the production or action of deleterious hormones. However, since metabolic acidosis accompanying CKD stimulates the secretion of several of these hormones, treatment of CKD should also include administration of base to correct the metabolic acidosis.

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Section: Aldosteronementioning

confidence: 99%

Section: Glucocorticoidsmentioning

confidence: 99%

The Role of the Endocrine System in the Regulation of Acid–Base Balance by the Kidney and the Progression of Chronic Kidney Disease

Nagami,

Kraut

2024

IJMS

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pH Homeostasis in Terrestrial Vertebrates: A Comparison of Traditional and New Concepts

Pörtner¹

1995

Mechanisms of Systemic Regulation: Acid—Base Regulation, Ion-Transfer and Metabolism

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Identification of the site of glucocorticoid action on neutral amino acid transport in superficial nephrons of rat kidney

2000

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Glucocorticoid hormones enhance the reabsorptive capacity of filtered amino acids in rat kidney, as it was shown in previous in vivo clearance experiments. In the present study, the site of glucocorticoid action on neutral amino acid transport in superficial nephrons of rat kidney was investigated using in vivo micropuncture technique. Adult female Wistar rats were treated with dexamethasone (DEX), and fractional excretion of L-glutamine (L-Gln) and L-leucine (L-Leu) were determined and related to inulin after microinfusion into different nephron segments. DEX reduced fractional excretion of both neutral amino acids as a sign of enhanced reabsorptive capacity. The site of main DEX action on L-Leu reabsorption has been localized in the proximal straight tubule. However, in the case of L-Gln, the inhibition of gamma-glutamyltranspeptidase (gamma-GT) by administration of acivicin indicated the importance of this brush border enzyme in reduced L-Gln excretion. DEX enhanced gamma-GT activity by tubular acidification. It can be presumed a DEX-inducible transport system for neutral amino acids mainly localized in proximal straight tubules of rat kidney.

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Glucocorticoid and Acid-Base Homeostasis: Effects on Glutamine Metabolism and Transport

Cited by 8 publications

References 12 publications

The Role of the Endocrine System in the Regulation of Acid–Base Balance by the Kidney and the Progression of Chronic Kidney Disease

The Role of the Endocrine System in the Regulation of Acid–Base Balance by the Kidney and the Progression of Chronic Kidney Disease

pH Homeostasis in Terrestrial Vertebrates: A Comparison of Traditional and New Concepts

Identification of the site of glucocorticoid action on neutral amino acid transport in superficial nephrons of rat kidney

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