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

Schwertfeger, M.; Roskos, Martin; Fleck, Christian

doi:10.1007/s007260050024

Cited by 5 publications

(4 citation statements)

References 24 publications

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“…Glucocorticoids have other important actions on renal function (e.g. downregulation of sodium/phosphate cotransport, 33 sulphate cotransport 34 and sodium effects on amino acid transport 35 ), as well as effects on acid–base, 36 including upregulation of the sodium/bicarbonate cotransporter, 37 but these effects are beyond the scope of the present review.…”

Section: Effects Of Cortisol On Renal Function and Renal Haemodynamicsmentioning

confidence: 94%

Glucocorticoids and the kidney

et al. 2003

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SUMMARY:Glucocorticoids are widely used by nephrologists for their immunomodulatory and anti-inflammatory effects. The present review considers three aspects of glucocorticoids with which nephrologists may be less familiar: (i) renal metabolism; (ii) effects on renal haemodynamics; and (iii) effects on blood pressure as they relate to the kidney.KEY WORDS: corticosterone, cortisol, dehydrogenase, haemodynamics, 11b b b b -hydroxysteroid, hypertension, metabolism, steroids.

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Section: Effects Of Cortisol On Renal Function and Renal Haemodynamicsmentioning

confidence: 94%

Glucocorticoids and the kidney

et al. 2003

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“…Broer et al [29] found increased 4F2hc mRNA levels and enhanced L-type amino acid transport activity in phorbol esters-treated lymphocytes. The glucocorticoid dexamethasone was found to induce both the activity and expression of 4F2hc in the rat kidney [2]. Arginine depletion increased TA1/LAT1 mRNA expression, accompanied with no appreciable response of 4F2hc in rat hepatic cell lines [30].…”

Section: Discussionmentioning

confidence: 93%

“…Steroid hormones have been shown to enhance or diminish amino acid transport depending on the nature of the hormone. Micropuncture studies revealed a glucocorticoidinducible transport system for neutral amino acids mainly located in proximal straight tubules of rat kidney [2]. Dexamethasone was found to induce both the activity and expression of transport system y + LAT1 [2,3].…”

Section: Introductionmentioning

confidence: 95%

“…Micropuncture studies revealed a glucocorticoidinducible transport system for neutral amino acids mainly located in proximal straight tubules of rat kidney [2]. Dexamethasone was found to induce both the activity and expression of transport system y + LAT1 [2,3]. ASUR4 is a Xenopus leavis LAT-type light chains reported to be induced at mRNA level by aldosterone in epithelial cells [4].…”

Section: Introductionmentioning

confidence: 99%

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Regulation of Renal LAT2 and 4F2hc Expression by Aldosterone

Pinho¹,

Amaral²,

Pinto³

et al. 2009

JEBP

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In the spontaneous hypertensive rat, overexpression of the renal Na +-independent L-amino acid transporter LAT2 is organ specific, precedes the onset of hypertension, correlates negatively with plasma aldosterone, and parallels the enhanced ability to take up L-DOPA and form renal dopamine. The present study evaluated the role of aldosterone on transcript and protein abundance of Na +-independent and Na +-dependent amino acid transporters. Na +-independent heterodimeric amino acid transporters LAT1/4F2hc, LAT2/4F2hc and a Na +-dependent transporter ASCT2 transcript and protein abundance was determined in the renal cortex of normotensive Wistar rats chronically treated with aldosterone (1.5 mg), spironolactone (200 mg) or aldosterone plus spironolactone. Aldosterone significantly increased renal cortical LAT2 mRNA levels (45 % increase), with no changes in LAT1, 4F2hc and ASCT2 transcript levels. The effect of aldosterone upon LAT2 mRNA levels was completely prevented by spironolactone. At the protein level, aldosterone treatment did not significantly affect LAT1 and LAT2 expression, but markedly reduced (51 % decrease) the abundance of 4F2hc and the urinary excretion of dopamine and DOPAC. The effect of aldosterone upon 4F2hc protein abundance was not reversed by spironolactone. Increases in renal LAT2 transcript during chronic treatment with aldosterone occur through a spironolactone-sensitive genomic mechanism. This effect parallels with a decrease in LAT2 functionality, resulting from decreases in 4F2hc protein abundance, which appears to be either a non-genomic effect or an indirect effect of aldosterone. The decrease in LAT2 functionality by aldosterone correlates well with the reduction in urinary dopamine.

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Regulation of renal amino acid (AA) transport by hormones, drugs and xenobiotics - a review

2003

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Major advances have recently been made in our understanding of the mechanisms and functions of amino acid transport in mammalian cells: - from the whole organism to transporter molecular structure. In this article, we present a brief overview of current knowledge concerning amino acid transporters, followed by a detailed discussion of the relevance of this new information to our broader understanding of the physiological regulation of amino acid handling in the kidney. We focus especially on the influence of hormones and xenobiotics on renal amino acid transport systems. In a growing number of cases, it now seems possible to correlate the effects of hormones, drugs, and xenobiotics with the capacity of renal amino acid transporters. This topic is of clinical relevance for the treatment of many amino acid reabsorption disorders. For example, under suitable conditions glucocorticoids and thyroid hormones stimulate renal reabsorption of amino acids and might therefore be of benefit in the treatment of different kinds of aminoaciduria. Hormonal regulation also underlies the postnatal development of renal amino acid reabsorption capacity, which can be stimulated to mature earlier after exogenous administration of e.g. glucocorticoids. In contrast, many compounds (e.g. heavy metal complexes) selectively damage renal amino acid transporters resulting in urinary amino acid loss. These types of phenomena (stimulation or inhibition of amino acid transporters in the kidney) are reviewed from the perspectives of our new molecular understanding of transport processes and of clinical relevance.

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

Cited by 5 publications

References 24 publications

Glucocorticoids and the kidney

Glucocorticoids and the kidney

Regulation of Renal LAT2 and 4F2hc Expression by Aldosterone

Regulation of renal amino acid (AA) transport by hormones, drugs and xenobiotics - a review

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