Effects of hypercalcemia on water and sodium excretion by the isolated dog kidney

Vanherweghem, Jean‐Louis; Ducobu, Jean; D’Hollander, Alain; Toussaint, C

doi:10.1007/bf00587405

Cited by 15 publications

(11 citation statements)

References 33 publications

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“…It is well known that hypercalcemia leads to a decrease in GFR, both acutely (11,12) and chronically (13 (27) that a decline in CA of the magnitude observed in the present study leads to an increase, rather than a decrease, in GFR. Therefore, the major factor responsible for the declines in GFR and SNGFR measured during acute hypercalcemia in non-TPTX rats was a profound reduction in Kf.…”

Section: Discussionsupporting

confidence: 56%

“…In addition, the calcium ion is capable of stimulating production of cGMP in several tissues (9), again including renal epithelia (10). Because elevation in plasma calcium concentration is well known to diminish glomerular filtration rate (GFR; [11][12][13], and because the calcium ion exerts a potent influence on cyclic nucleotide production and action, we undertook the present series of investigations to explore the effects of acute hypercalcemia on the determinants of GFR. T Proximal tubule.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Evidence for a parathyroid hormone-dependent influence of calcium on the glomerular ultrafiltration coefficient.

Humes¹,

Ichikawa²,

Troy³

et al. 1978

J. Clin. Invest.

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A B S T R A C T Experiments were performed on 36 plasma-expanded Munich-Wistar rats to examine the effects of acute hypercalcemia on the determinants of glomerular ultrafiltration. Elevation of total plasma calcium concentration to an average value of 13.2±0.5 mg/dl, by acute infusion of calcium chloride into nonthyroparathyroidectomized (non-TPTX) rats, resulted in significant declines in single nephron and whole kidney glomerular filtration rate. These declines were due primarily to a fall in the glomerular capillary ultrafiltration coefficient (Kf), to a mean value approximately 60% below that determined in the preinfusion period. These changes were not seen in a separate group of sham-treated non-TPTX rats.It is of interest that these effects of acute hypercalcemia were largely abolished in rats that underwent acute TPTX before hypercalcemia. Infusion of a submaximally phosphaturic dose of parathyroid hormone, together with calcium chloride, into a second group of acute TPTX rats, however, had the effect of reproducing the striking declines in filtration rate and Kf noted in non-TPTX rats given calcium chloride alone. These findings suggest that the decline in filtration rate associated with hypercalcemia is due largely to the reduction in Kf,, the latter dependent upon the presence of parathyroid hormone.Portions of these studies were presented at the annual

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Section: Discussionsupporting

confidence: 56%

Section: Introductionmentioning

confidence: 99%

Evidence for a parathyroid hormone-dependent influence of calcium on the glomerular ultrafiltration coefficient.

Humes¹,

Ichikawa²,

Troy³

et al. 1978

J. Clin. Invest.

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“…The fact that acute and chronic hypercalcemia cause a decreased RBF and GFR in both man and experimental animals has been repeatedly reported (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15) (35)(36)(37)(38).…”

Section: Discussionmentioning

confidence: 94%

“…The association of acute and chronic hypercalcemia with decrements in renal blood flow (RBF)' and glomerular filtration rate (GFR) has been widely recognized in both man and experimental animals (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15). While the mechanisms responsible for the decrement in RBF and GFR have been studied in anesthetized, acutely hypercalcemic animals, there have been no such studies in the setting of chronic hypercalcemia.…”

mentioning

confidence: 99%

Control of Renal Hemodynamics and Glomerular Filtration Rate in Chronic Hypercalcemia

Levi¹,

Ellis²,

Berl³

1983

J. Clin. Invest.

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A B S T R A C T The role of prostaglandins (PG), reninangiotensin system (RAS) and calcium (Ca) in the control of renal hemodynamics and glomerular filtration rate (GFR) in chronic hypercalcemia (serum Ca 12.8 mg%) was studied. Renal blood flow (RBF, 6.39 ml/ min per gram kidney weight [gkw]) and GFR (0.52 ml/min per gkw) were significantly decreased in hypercalcemic rats when compared with normocalcemic rats (7.15, P < 0.001 and 0.74, P < 0.05, respectively). These changes in RBF and GFR occurred independent of any significant alterations in systemic hemodynamics, blood and plasma volume. Inhibition of the renal PG with indomethacin resulted in marked decrements in both RBF (6.39-4.12 ml/min per gkw, P < 0.01) and GFR (0.52-0.19 ml/min per gkw, P < 0.01) in hypercalcemic rats, whereas there was no significant alterations in normocalcemic rats. Inhibition of the RAS with captopril resulted in marked increments in both RBF (6.39-7.35 ml/min per gkw, P < 0.05) and GFR (0.52-0.74 ml/min per gkw, P < 0.05) in hypercalcemic rats. In fact, there was no significant difference from the RBF and GFR of similarly treated normocalcemic rats. Similar results were also obtained with the competitive angiotensin II (AII) antagonist (sarcosyll-isoleucyl5-glycyl8) AII. Since both the renal PG and the RAS are involved in the control of RBF and GFR in hypercalcemia, the role of each is best revealed in the absence of the other. Hence, comparison of the RBF and GFR in the PG-inhibited hypercalcemic rats in the presence of AII (4.12 and 0.19 ml/ min per gkw, respectively) and absence of AII (5.99 and 0.53 ml/min per gkw, P < 0.01 for both) reveals the vasoconstrictive role for All in hypercalcemia. On the other hand, comparison of the RBF and GFR in the AII-inhibited hypercalcemic rats in the presence of PG (7.35 and 0.74 ml/min per gkw, respectively) and absence of PG (5.99 and 0.53 ml/min per gkw, P < 0.01 and P < 0.05, respectively) reveals the vasodilatory role for PG in hypercalcemia. Finally, comparison of the RBF and GFR in both PG-and Allinhibited hypercalcemic rats (5.99 and 0.53 ml/min per gkw, respectively) with similarly treated normocalcemic rats (7.30 and 0.94 ml/min per gkw, P < 0.001 and P < 0.005, respectively) reveals the vasoconstrictive role for Ca in chronic hypercalcemia. Our study therefore demonstrates that in chronic hypercalcemia the RBF and GFR are controlled by an active interplay of the vasoconstrictive effect of AII, the vasodilatory effect of renal PG, and the direct vasoconstrictive effect of Ca, independent of either AII or PG. The sum total of these forces produces a modest but significant decrease in RBF and GFR. INTRODUCTIONThe association of acute and chronic hypercalcemia with decrements in renal blood flow (RBF)' and glomerular filtration rate (GFR) has been widely recognized in both man and experimental animals (1-15). While the mechanisms responsible for the decrement in RBF and GFR have been studied in anesthetized, acutely hypercalcemic animals, there have been no such studies in the setting...

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“…3-4 mmol 1-1 or more) has been shown to increase water and electrolyte excretion (Levitt, Halpern, Polimeros, Sweet & Gribetz, 1958;Epstein, 1968;Vanherweghem, Ducobu, D'Hollander & Toussaint, 1976;Lins, 1979a, b). In broad terms, the parallel changes in sodium and calcium clearance have been attributed to the mainly passive (solvent drag and electrochemical differences), and indirectly sodium-related, proximal tubular reabsorption of calcium (Sutton & Dirks, 1978;Dennis, Stead & Myers, 1979;Suki, 1979).…”

Section: Introductionmentioning

confidence: 99%

Renal electrolyte excretion and renin release during calcium and parathormone infusions in conscious rabbits.

Peart¹,

Roddis²,

Unwin³

1986

The Journal of Physiology

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SUMMARY1. Following a random block experimental design in each case, three repeated measurement studies were carried out in three different groups of conscious rabbits, to investigate the renal effects of increasing doses of intravenous calcium chloride (CaC12) and bovine parathyroid hormone (PTH).2. In the first study, each rabbit received either CaCl2 (0415, 0 3, 0-5 or 1D0 mg kg-' min-) or vehicle alone (control) for 160 min. In the second study, rabbits were given either PTH (0415 ,ug kg-' min'), CaCl2 (1D0 mg kg-' min-), PTH plus CaCl2 (0415 jug kg-' min-and 1-0 mg kg-' min-, respectively) or vehicle alone; PTH was infused for just over 60 min. In the third study, a much smaller dose (005 mg kg-' min-) of CaCl2 was infused for 100 min.3. CaCl2 infusion produced a striking fall in fractional excretion of sodium of at least 50 % (P < 0-01), but this was not dose related, being almost maximal at the smaller doses infused. Although this effect was evident in the absence of any changes in total plasma calcium concentration at the lower doses of CaCl2, renal calcium excretion was increased between 2-and 20-fold (P < 001) at all doses infused. Fractional excretion of chloride doubled at the two higher doses of CaCl2 (P < 0.01), but potassium excretion was unchanged. There were no consistent alterations in mean arterial blood pressure, effective renal plasma flow, glomerular filtration rate or plasma renin activity (PRA); total plasma calcium concentration was consistently elevated only during infusion of the high dose by just under 1 mmol 1-1.4. PTH infusion had no measured effect on fractional excretion of sodium or renal calcium excretion, but doubled fractional potassium excretion (P < 0 05). Heart rate and PRA increased (P < 0-01 and < 0-05, respectively), the latter by 50 %, but systemic pressure and renal haemodynamics were not significantly affected. By contrast, PTH infused with CaCl2 produced a 4-fold rise in fractional sodium excretion and although renal calcium excretion remained increased, it was reduced by ca. 80 % when compared with renal calcium excretion during infusion of CaCl2 alone. Infusion of PTH alone increased PRA, but when PTH and CaCl2 were infused together, PRA did not change.5. These observations are not fully explained, but may involve PTH-related changes in renal tubular and juxtaglomerular cell permeability to calcium, cytosolic calcium concentration and a sodium-calcium exchange process.

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Effects of hypercalcemia on water and sodium excretion by the isolated dog kidney

Cited by 15 publications

References 33 publications

Evidence for a parathyroid hormone-dependent influence of calcium on the glomerular ultrafiltration coefficient.

Evidence for a parathyroid hormone-dependent influence of calcium on the glomerular ultrafiltration coefficient.

Control of Renal Hemodynamics and Glomerular Filtration Rate in Chronic Hypercalcemia

Renal electrolyte excretion and renin release during calcium and parathormone infusions in conscious rabbits.

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