Changes in inorganic phosphate excretion induced by renal arterial infusion of calcium

Lavender, A. R.; Pullman, Theodore N.

doi:10.1152/ajplegacy.1963.205.5.1025

Cited by 81 publications

(22 citation statements)

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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).…”

Section: Discussionmentioning

confidence: 98%

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: Discussionmentioning

confidence: 98%

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

et al. 1974

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“…However, the benefit obtained from temporary restoration of extracellular calcium levels by calcium infusion as demonstrated in this study and elsewhere [lo], indicates that another mechanism for the tubular dysfunction may exist. LAVENDER and PULLMAN [31] have proposed that calcium ion may itself enhance tubular transport of phosphorus; they did not study the effect of this ion on amino acid absorption. However, the suppresive action of calcium upon synthesis and release of parathyroid hormone must also be considered [3 1,361.…”

Section: Discussionmentioning

confidence: 99%

Hyperparathyroidism as the Cause of Hyperaminoaciduia and Phosphaturia in Human Vitamin D Deficiency

1967

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ExtractThirty-nine infants with simple vitamin D deficiency were studied; three stages of deficiency were recognized. Stage I comprised hypocalcemia, usually as the sole important biochemical finding, while convulsions were a common clinical sign. Stage I1 revealed normocalcemia with hyperaminoaciduria, hypophosphatemia, and hyperphosphaturia; rickets was also in evidence. Stage I11 was comparable to stage 11, but with recurrence of hypocalcemia and convulsions, the rickets was more severe. Patients progressed spontaneously from the early to the later stages of the deficiency syndrome; administration of parathyroid extract appeared to accelerate the rate of progression. Calcium infusion and vitamin D therapy each initially raised the serum calcium level in hypocalcemic patients; thereafter, aminoaciduria and hyperphosphaturia were suppressed.These diverse observations were interpreted in accordance with current knowledge of vitamin D and parathyroid hormone interrelations. The acquired excretory abnormality involving amino acid and phosphorus is the result of impaired tubular absorption; this defect is considered to be dependent on the development of endogenous reactive hyperparathyroidism, and not dependent on cellular deficiency of vitamin Dper se. The stimulus for the hyperparathyroidism is hypocalcemia induced by deficiency of vitamin D. Normocalcemia is restored if sufficient vitamin D is present in cellular membranes to amplify the stimulative action of parathyroid hormone on intestinal transport of calcium and its release from bone. Severe deficiency of vitamin D blocks this regulatory effect upon calcium, but does not block the inhibitory effect of parathyroid hormone on renal tubular transport of amino acids and phosphorus. SpeculationAn excess of parathyroid hormone rather than a simple deficiency of vitamin D at the renal tubular epithelial cell appears to cause the disturbance of transport affecting the absorption phosphorus, amino acids and other solutes. This impairment of function is the price paid in renal cellular economy for the conservation of calcium. The cellular mechanisms underlying this coexistent inhibitory effect of parathyroid hormone constitutes an important and fascinating subject for further investigation.

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“…Calcium infusion has been reported both to increase (17) and to decrease (18) Pi reabsorption, and hypercalcemia has been reported to reduce the phosphaturic response to volume expansion in the rat (19). In our two groups of acute TPTX rats, control plasma calcium values were similar, but plasma calcium decreased substantially during phosphate infusion in the lowphosphorus dietary group.…”

Section: Resultsmentioning

confidence: 99%

“…In our two groups of acute TPTX rats, control plasma calcium values were similar, but plasma calcium decreased substantially during phosphate infusion in the lowphosphorus dietary group. If Pi reabsorption varies directionally with the plasma calcium (17,19), then Pi reabsorption in the low-phosphorus acute TPTX rats might have been impaired secondary to hypocalcemia during late phosphate infusion. Within the chronic TPTX groups, plasma calcium was initially greater in the low-phosphorus rats, but values in the two groups became nearly equal by late phosphate infusion.…”

Section: Resultsmentioning

confidence: 99%

Influence of dietary phosphorus on renal phosphate reabsorption in the parathyroidectomized rat.

Steele¹,

DeLuca²

1976

J. Clin. Invest.

142

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Changes in inorganic phosphate excretion induced by renal arterial infusion of calcium

Cited by 81 publications

References 0 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

Hyperparathyroidism as the Cause of Hyperaminoaciduia and Phosphaturia in Human Vitamin D Deficiency

Influence of dietary phosphorus on renal phosphate reabsorption in the parathyroidectomized rat.

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