Phosphate transport in the light segment of the rabbit cortical collecting tubule

Shareghi, G. R.; Agus, Z. S.

doi:10.1152/ajprenal.1982.242.4.f379

Cited by 10 publications

(5 citation statements)

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“…The decrease in this peak with prolonged obstruction in the unilateral model is almost certainly due to the reabsorption of urine and normalization oftubular pressures seen in this model (13,16,17). The demonstrated capacity of distal tubular segments to reabsorb Pi supports this contention (31)(32)(33)(34)(35). Other interesting observations can be drawn from our data.…”

Section: Statisticssupporting

confidence: 71%

P-31 nuclear magnetic resonance spectroscopic study of obstructive uropathy in the rat.

Shapiro¹,

Chan²

1987

J. Clin. Invest.

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Section: Statisticssupporting

confidence: 71%

P-31 nuclear magnetic resonance spectroscopic study of obstructive uropathy in the rat.

Shapiro¹,

Chan²

1987

J. Clin. Invest.

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“…Estimations from micropuncture studies suggest little Mg 2+ transport after the DCT. Microperfusion of cortical CDs failed to show a significant amount of net Mg 2+ movement [201]. In line with this, microcatheterization studies found no net Mg 2+ transport over the length of the inner medulla CD [202].…”

Section: Collecting Systemsupporting

confidence: 53%

Hereditary tubular transport disorders: implications for renal handling of Ca2+ and Mg2+

2009

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The kidney plays an important role in maintaining the systemic Ca2+ and Mg2+ balance. Thus the renal reabsorptive capacity of these cations can be amended to adapt to disturbances in plasma Ca2+ and Mg2+ concentrations. The reabsorption of Ca2+ and Mg2+ is driven by transport of other electrolytes, sometimes through selective channels and often supported by hormonal stimuli. It is, therefore, not surprising that monogenic disorders affecting such renal processes may impose a shift in, or even completely blunt, the reabsorptive capacity of these divalent cations within the kidney. Accordingly, in Dent's disease, a disorder with defective proximal tubular transport, hypercalciuria is frequently observed. Dysfunctional thick ascending limb transport in Bartter's syndrome, familial hypomagnesaemia with hypercalciuria and nephrocalcinosis, and diseases associated with Ca2+-sensing receptor defects, markedly change tubular transport of Ca2+ and Mg2+. In the distal convolutions, several proteins involved in Mg2+ transport have been identified [TRPM6 (transient receptor potential melastatin 6), proEGF (pro-epidermal growth factor) and FXYD2 (Na+/K+-ATPase gamma-subunit)]. In addition, conditions such as Gitelman's syndrome, distal renal tubular acidosis and pseudohypoaldosteronism type II, as well as a mitochondrial defect associated with hypomagnesaemia, all change the renal handling of divalent cations. These hereditary disorders have, in many cases, substantially increased our understanding of the complex transport processes in the kidney and their contribution to the regulation of overall Ca2+ and Mg2+ balance.

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“…Mg 2ϩ transport in the CD appears to be absent. Microperfusion experiments on rabbit cortical CD could not detect significant Mg 2ϩ flux (217). Furthermore, the microcatherization studies outlined above failed to find significant absorption of Mg 2ϩ along the inner medullary CD (21).…”

Section: Transcellular Transport Of Ca 2ϩ and Mg 2ϩ In The Distal Convolution And Collecting Systemmentioning

confidence: 88%

Effect of diuretics on renal tubular transport of calcium and magnesium

Alexander

Dimke

2017

American Journal of Physiology-Renal Physiology

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Calcium (Ca) and Magnesium (Mg) reabsorption along the renal tubule is dependent on distinct trans- and paracellular pathways. Our understanding of the molecular machinery involved is increasing. Ca and Mg reclamation in kidney is dependent on a diverse array of proteins, which are important for both forming divalent cation-permeable pores and channels, but also for generating the necessary driving forces for Ca and Mg transport. Alterations in these molecular constituents can have profound effects on tubular Ca and Mg handling. Diuretics are used to treat a large range of clinical conditions, but most commonly for the management of blood pressure and fluid balance. The pharmacological targets of diuretics generally directly facilitate sodium (Na) transport, but also indirectly affect renal Ca and Mg handling, i.e., by establishing a prerequisite electrochemical gradient. It is therefore not surprising that substantial alterations in divalent cation handling can be observed following diuretic treatment. The effects of diuretics on renal Ca and Mg handling are reviewed in the context of the present understanding of basal molecular mechanisms of Ca and Mg transport. Acetazolamide, osmotic diuretics, Na/H exchanger (NHE3) inhibitors, and antidiabetic Na/glucose cotransporter type 2 (SGLT) blocking compounds, target the proximal tubule, where paracellular Ca transport predominates. Loop diuretics and renal outer medullary K (ROMK) inhibitors block thick ascending limb transport, a segment with significant paracellular Ca and Mg transport. Thiazides target the distal convoluted tubule; however, their effect on divalent cation transport is not limited to that segment. Finally, potassium-sparing diuretics, which inhibit electrogenic Na transport at distal sites, can also affect divalent cation transport.

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Phosphate transport in the light segment of the rabbit cortical collecting tubule

Cited by 10 publications

References 0 publications

P-31 nuclear magnetic resonance spectroscopic study of obstructive uropathy in the rat.

P-31 nuclear magnetic resonance spectroscopic study of obstructive uropathy in the rat.

Hereditary tubular transport disorders: implications for renal handling of Ca2+ and Mg2+

Effect of diuretics on renal tubular transport of calcium and magnesium

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