Micropuncture Studies of Phosphate Transport in the Proximal Tubule of the Dog THE RELATIONSHIP TO SODIUM REABSORPTION

Wen, Sung-Feng

doi:10.1172/jci107532

Cited by 87 publications

(41 citation statements)

References 53 publications

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“…Lavender and Pullman have also observed increased phosphate absorption when they infused calcium into the renal artei ies of dogs (38). Wen, on the other hand, could not detect a decrease in phosphate clearance after the infusion of CaCL into dogs (39). Also at variance with our studies are the observations of Eisenberg (40) who reported increased clearance of phosphate after infusion of calcium for 72 h in hypoparathyroid patients.…”

Section: Discussioncontrasting

confidence: 69%

Effects of Volume Expansion, Purified Parathyroid Extract, and Calcium on Renal Bicarbonate Absorption in the Dog

et al. 1974

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A B S T R A C T The role of parathyroid hormone (PTH) and of Ca++ in the regulation of bicarbonate absorption (RHCO3) and its response to extracellular volume expansion (VE) was studied in HC03-loaded dogs.VE lowered RHCO3 in both intact (from 24.8 to 22.0 mmol/liter GFR, P < 0.01) and thyroparathyroidectomized (TPTX) (from 24.5 to 18.0 mmol/liter GFR, P < 0.001) dogs; glomerular filtration rate (GFR) and filtered HCOi-did not change. Both groups showed a significant increase in the fractional excretion of sodium (CNa X 100/GFR), calcium (CCa X 100/ GFR), and chloride (Cci X 100/GFR) and a decrease in phosphorus reabsorption. Fractional clearance of phosphate (CP X 100/GFR) rose in both groups but did not achieve significance.Infusion of purified parathyroid extract (PTE) decreased RHCOs in intact dogs (from 24.6 to 22.5 mmol/ liter GFR, P < 0.025) and in TPTX dogs (from 26.9 to 22.6 mmol/liter GFR, P < 0.05). No Infusion of Ca++ raised ultrafilterable Ca++ from 5.7 to 7.9 mg/100 ml in intact and from 4.9 to 7.2 mg/ 100 ml in TPTX dogs; RHCOs increased in intact (from 22.9 to 26.9 mmol/liter GFR, P < 0.025) and in TPTX dogs (from 26.6 to 28.6 mmol/liter GFR, P <0.05). The GFR, RBF, and the fractional excretion of sodium, chloride, and calcium did not change in either group. The reabsorbed phosphate increased in both groups, and fractional phosphorus clearance fell in the intact group but did not change significantly in the TPTX group.Superimposition of PTE on hypercalcemia in TPTX dogs resulted in a decrease in RHco8 (from 27.3 to 23.9 mmol/liter GFR, P < 0.001), which was accompanied by an increase in the fractional excretion of phosphate and a decrease in the reabsorbed phosphate. In this group of TPTX dogs hypercalcemia caused a drop in RBF from 135.6 to 105.8 ml/min with no change in GFR. The RBF returned to control value with PTE infusion.It is concluded that: (a) the lowering of RHCO3 by VE is not dependent solely on stimulation of PTH by the lowered Ca', (b) PTE acts directly on the renal tubules to lower RHCOs, (c) Ca' enhances RHcos and this effect is exerted in the absence of PTH and calcitonin, (d) neither the effects of CaZ nor of PTH appear to be mediated by altered hemodynamics, although this cannot be excluded in Ca^-infused TPTX dogs, (e) Ca' enhanced phosphate reabsorption in the absence of PTH; this may be a specific effect of hypercalcemia on phosphate reabsorption or the nonspecific consequence of the rise in serum phosphorus.

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Section: Discussioncontrasting

confidence: 69%

Effects of Volume Expansion, Purified Parathyroid Extract, and Calcium on Renal Bicarbonate Absorption in the Dog

et al. 1974

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“…Volume expansion per se has subsequently been shown to reduce proximal phosphate reabsorption (8,9,31,32). Furthermore, administration of acetazolamide, which tends to lower the in situ pH in the proximal tubule (21), also results in inhibition of phosphate reabsorption (10,11,30). This latter effect has recently been attributed to stimulation of renal adenyl cyclase by acetazolamide (33), a mechanism of action thought to be similar to that of PTH (5).…”

Section: Resultsmentioning

confidence: 99%

“…Recent micropuncture studies have demonstrated several important features of the renal reabsorptive process for inorganic phosphate (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11). First, the proximal tubule is responsible for most but not all of phosphate reabsorption, the most avid site being the early portion of the proximal convoluted tubule (2,4).…”

Section: Introductionmentioning

confidence: 99%

“…First, the proximal tubule is responsible for most but not all of phosphate reabsorption, the most avid site being the early portion of the proximal convoluted tubule (2,4). Second, phosphate reabsorption has been found to parallel fluid reabsorption in the proximal tubule under certain experimental conditions (5)(6)(7)(8)(9)(10)(11). For example, extracellular fluid volume expansion results in a reduction in proximal sodium, water, and phosphate reabsorption (8,9,11).…”

Section: Introductionmentioning

confidence: 99%

“…Second, phosphate reabsorption has been found to parallel fluid reabsorption in the proximal tubule under certain experimental conditions (5)(6)(7)(8)(9)(10)(11). For example, extracellular fluid volume expansion results in a reduction in proximal sodium, water, and phosphate reabsorption (8,9,11). Third, the inhibition of phosphate reabsorption by parathyroid hormone (PTH)1 may be linked to an inhibitory action of the hormone on proximal fluid reabsorption (5-7), although it is possible to dissociate the two effects (11).…”

Section: Introductionmentioning

confidence: 99%

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A Microperfusion Study of Phsophate Reabsorption by the Rat Proximal Renal Tubule EFFECT OF PARATHYROID HORMONE

Bank¹,

Aynedjian²,

Weinstein³

1974

J. Clin. Invest.

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A B S T R A C T To study the mechanism of phosphate reabsorption by the proximal tubule and the effect of parathyroid hormone (PTH), microperfusion experiments were carried out in rats. Segments of proximal tubule isolated by oil blocks were perfused in vivo with one of three solutions, each containing 152 meq/liter Na' and 2 mmol/liter phosphate, but otherwise differing in composition. The pH of solution 1 was 6.05-6.63, indicating that 60-85% of the phosphate was in the form of H2PO4. The pH of solution 2 was 7.56-7.85, and 85-92% of the phosphate was in the form of HP04=. Solution 3 contained HC03-and glucose and had a pH of 7.50-7.65. When the proximal tubules were perfused with solution 1, the "2P concentration in the collected perfusate was found to be consistently lower than in the initial perfusion solution. In sharp contrast, when the tubules were perfused with solutions 2 or 3, s'P concentration usually rose above that in the initial solution. Water (and presumably Na') reabsorption, as measured with ['H]inulin, was the same with the acid and alkaline solutions. Administration of partially purified PTH clearly prevented the fall in phosphate concentration with the acid solution, but had a less discernible effect on phosphate reabsorption with the two alkaline solutions. Measurements of pH within the perfused segments with antimony microelectrodes demonstrated that PTH enhanced alkalinization of the acid perfusion solution. The findings are consistent with the view that H2POf is reabsorbed preferentially over HPO4=. This can be attributed to either an active transport mechanism for H2PO4J or selective membrane permeability to this anion. PTH appears to either inhibit an active transport process for H2PO4-, or to interfere with pas-

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Treatment of Bartter's Syndrome With Indomethacin

Garin¹

1980

Arch Pediatr Adolesc Med

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\s=b\Two patients with Bartter's syndrome were treated with indomethacin (2 mg/ kg/day). The administration of the drug resulted in weight gain; a decrease in the rate of urinary excretion of sodium and inorganic phosphate suggesting an increase in proximal tubular reabsorption; an increase in serum potassium concentration, with a transient decrease in the rate of urinary potassium excretion in one patient; and a decrease in plasma renin activity and in the rate of urinary aldosterone excretion. Since indomethacin has been shown to inhibit prostaglandin synthetase, these observations support the hypothesis that prostaglandin excess is a basic pathogenic mechanism in Bartter's syndrome. (Am J Dis Child 134:258-261, 1980)

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Micropuncture Studies of Phosphate Transport in the Proximal Tubule of the Dog THE RELATIONSHIP TO SODIUM REABSORPTION

Cited by 87 publications

References 53 publications

Effects of Volume Expansion, Purified Parathyroid Extract, and Calcium on Renal Bicarbonate Absorption in the Dog

Effects of Volume Expansion, Purified Parathyroid Extract, and Calcium on Renal Bicarbonate Absorption in the Dog

A Microperfusion Study of Phsophate Reabsorption by the Rat Proximal Renal Tubule EFFECT OF PARATHYROID HORMONE

Treatment of Bartter's Syndrome With Indomethacin

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