The Hormonal and Non-Hormonal Control of Renal Excretion of Calcium and Magnesium

Massry, Shaul G.; Jw, Coburn

doi:10.1159/000180181

Cited by 94 publications

(38 citation statements)

References 158 publications

(235 reference statements)

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“…Previous immunohistochemical studies in mouse kidney indeed indicated that TRPM6 is localized exclusively along the apical domain in DCT, which is in line with the postulated gatekeeper function in the process of active Mg 2ϩ reabsorption (13 excretion without significant increases in plasma Mg 2ϩ , which is in accordance with the results of our study in mouse (27 increased urinary Ca 2ϩ excretion. In accordance with this finding, Shafik and Quamme (7) showed that urinary Ca 2ϩ excretion decreases in rats that are maintained on a low-Mg 2ϩ diet.…”

Section: Discussionsupporting

confidence: 92%

The Epithelial Mg2+ Channel Transient Receptor Potential Melastatin 6 Is Regulated by Dietary Mg2+ Content and Estrogens

Groenestege¹,

Hoenderop²,

Heuvel

et al. 2006

Journal of the American Society of Nephrology

219

198

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Section: Discussionsupporting

confidence: 92%

The Epithelial Mg2+ Channel Transient Receptor Potential Melastatin 6 Is Regulated by Dietary Mg2+ Content and Estrogens

Groenestege¹,

Hoenderop²,

Heuvel

et al. 2006

Journal of the American Society of Nephrology

219

198

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“…This response is rapid, occurring within 4-8 hours; is sensitive, proceeds without a detectable change in plasma magnesium concentration; and is selective in the long term, altering magnesium reabsorption without changes in Na + or Ca 2+ excretion. Conversely in states of magnesium surfeit, urinary magnesium markedly increases without significant increases in plasma magnesium (101). This ability to adapt to magnesium availability is intrinsic as it may be observed in isolated cells independent of hormones and other factors (60, 61).…”

Section: Intrinsic Control: Magnesium Restrictionmentioning

confidence: 99%

“…The Ca 2+ /Mg 2+ -sensing receptor also explains the so-called "Tm" phenomenon of urinary magnesium excretion (101,(120)(121)(122). Clearance studies have suggested that renal magnesium reabsorption is a Tmlimited process, i.e.…”

Section: 2ca2+/mg2+-sensing:hypercalcemia Hypermagnesemiamentioning

confidence: 99%

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Epithelial magnesium transport and regulation by the kidney

C²

2000

Front Biosci

102

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Magnesium is the fourth most abundant cation in the body and the second most common cation in the intracellular fluid. It is the kidney that provides the most sensitive control for magnesium balance. About a 80% of the total serum magnesium is ultrafilterable through the glomerular membrane. In all of the mammalian species studied to date, the proximal tubule of the adult animal reabsorbs only a small fraction, 10-15%, of the filtered magnesium. Unlike the adult proximal convoluted tubule that of young rats (aged 13-15 days) reabsorbs 50-60% of filtered magnesium along the proximal tubule together with sodium, calcium, and water. Micropuncture experiments, in every species studied to date, indicates that a large part (approximately 60%) of the filtered magnesium is reabsorbed in the loop of Henle. Magnesium reabsorption in the loop occurs within the cortical thick ascending limb (cTAL) by passive means driven by the transepithelial voltage through the paracellular pathway. Micropuncture experiments have clearly showed that the superficial distal tubule reabsorbs significant amounts of magnesium. Unlike the thick ascending limb of the loop of Henle, magnesium reabsorption in the distal tubule is transcellular and active in nature. Many hormones and nonhormonal factors influence renal magnesium reabsorption to variable extent in the cTAL and distal tubule. Moreover, nonhormonal factors may have important implications on hormonal controls of renal magnesium conservation. Dietary magnesium restriction leads to renal magnesium conservation with diminished urinary magnesium excretion. Adaptation of magnesium transport with dietary magnesium restriction occurs in both the cTAL and distal tubule. Elevation of plasma magnesium or calcium concentration inhibits magnesium and calcium reabsorption leading to hypermagnesiuria and hypercalciuria. The

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“…In other studies also, bladder tumours occurred preferentially in male rats fed high levels of saccharin (Taylor & Friedman, 1974;Tisdel et al, 1974;Arnold et al, 1979) but there was no consistent relationship between urolithiasis and bladder tumours. Discrepancies in urolithiasis between different studies could reflect variation in dietary cation, carbohydrate or protein content, all of which may affect urine composition (Andersen, 1962;Lyon et al, 1966;Woodard, 1971;Massry & Coburn, 1973). The urolithiasis associated with our 3 bladder tumours consisted of free-lying calculi and/or mineralized deposits adherent to or within the tumours.…”

Section: Discussionmentioning

confidence: 90%

Response of the rat to saccharin with particular reference to the urinary bladder

Chowaniec¹,

Hicks²

1979

Br J Cancer

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Summary.-Male and female Wistar rats were administered sodium saccharin for life (2 yr) either in the drinking water or diet. The maximum palatable dose of saccharin in the drinking water was found to be 2 g/kg/day and, even then, there was some voluntary restriction of fluid intake in the males. By contrast, double this dose -namely 4 g/kg/day, was palatable in the diet. A control group of rats of both sexes received saccharin-free diet and drinking water. Mild urothelial hyperplasias developed from 85 weeks in rats of both sexes receiving saccharin either in the drinking water or diet; the incidence was statistically significant in both the bladders and kidneys of rats receiving the higher dose of saccharin in the diet, but in the kidneys only of rats receiving the lower dose of saccharin in the drinking water. Telangiectasia of the vasa recta was significant in saccharin-treated rats of both sexes at both doses. A very low incidence of bladder tumours, exclusively in males receiving the higher saccharin dose in the diet was seen from 95 weeks. No consistent relationship between bladder epithelial hyperplasias and crystalluria could be demonstrated, although all 3 bladder tumours were associated with some form of mineralisation. Results suggest a particular susceptibility of males to saccharin treatment. The possibility that saccharin may promote, or enhance, the development of latent tumour cells already present in the experimental population, rather than initiate carcinogenesis per se is considered.

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The Hormonal and Non-Hormonal Control of Renal Excretion of Calcium and Magnesium

Cited by 94 publications

References 158 publications

The Epithelial Mg2+ Channel Transient Receptor Potential Melastatin 6 Is Regulated by Dietary Mg2+ Content and Estrogens

The Epithelial Mg2+ Channel Transient Receptor Potential Melastatin 6 Is Regulated by Dietary Mg2+ Content and Estrogens

Epithelial magnesium transport and regulation by the kidney

Response of the rat to saccharin with particular reference to the urinary bladder

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