Effect of sodium bicarbonate on phosphate excretion in acute and chronic PTX rats

Zilenovski, A. M.; Kuroda, Shigetoshi; Bhat, Shahnawaz Ali; Bank, De; Bank, Norman

doi:10.1152/ajprenal.1979.236.2.f184

Cited by 5 publications

(3 citation statements)

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“…69,70 We also observed a brisk increase in phosphate excretion during the alkaline challenge, which gradually returned towards baseline during subsequent acidic load (Figure 5C). Phosphaturia during alkalosis is in line with previous observations in rats, 38,[43][44][45][46] dogs, 37,39,40 and humans. 41,42 The underlying mechanism is not exactly clear.…”

Section: Response To Dynamic Acid-base Challengesupporting

confidence: 91%

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Two‐pore channel protein TPC1 is a determining factor for the adaptation of proximal tubular phosphate handling

et al. 2023

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Aim Two‐pore channels (TPCs) constitute a small family of cation channels expressed in endo‐lysosomal compartments. TPCs have been characterized as critical elements controlling Ca2+‐mediated vesicular membrane fusion and thereby regulating endo‐lysosomal vesicle trafficking. Exo‐ and endocytotic trafficking and lysosomal degradation are major mechanisms of adaption of epithelial transport. A prime example of highly regulated epithelial transport is the tubular system of the kidney. We therefore studied the localization of TPC protein 1 (TPC1) in the kidney and its functional role in the dynamic regulation of tubular transport. Methods Immunohistochemistry in combination with tubular markers were used to investigate TPC1 expression in proximal and distal tubules. The excretion of phosphate and ammonium, as well as urine volume and pH were studied in vivo, in response to dynamic challenges induced by bolus injection of parathyroid hormone or acid–base transitions via consecutive infusion of NaCl, Na2CO3, and NH4Cl. Results In TPC1‐deficient mice, the PTH‐induced rise in phosphate excretion was prolonged and exaggerated, and its recovery delayed in comparison with wildtype littermates. In the acid–base transition experiment, TPC1‐deficient mice showed an identical rise in phosphate excretion in response to Na2CO3 compared with wildtypes, but a delayed NH4Cl‐induced recovery. Ammonium‐excretion decreased with Na2CO3, and increased with NH4Cl, but without differences between genotypes. Conclusions We conclude that TPC1 is expressed subapically in the proximal but not distal tubule and plays an important role in the dynamic adaptation of proximal tubular phosphate reabsorption towards enhanced, but not reduced absorption.

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Section: Response To Dynamic Acid-base Challengesupporting

confidence: 91%

“…Function and apical expression of NHE3 is augmented during acidosis and diminished during alkalosis 24,25 . In contrast, expression of NaPiIIa and phosphate reabsorption are reduced during acidosis leading to phosphaturia, 17,25 while alkalosis is also associated with phosphaturia 37–46 …”

Section: Discussionmentioning

confidence: 99%

Two‐pore channel protein TPC1 is a determining factor for the adaptation of proximal tubular phosphate handling

et al. 2023

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“…The same conclusion regarding volume expansion was reached in other studies carried out in dogs and man with intact parathyroid glands [9,13,16,20], Sodium bicarbonate infusion lowers total and ionized serum calcium concentration [18], and, in the TPTX rat, hypocalcemia has been shown to inhibit renal phosphate reabsorption [1,21]. Although an effect of hypocalcemia in inhibiting phosphate reab sorption cannot be ruled out in the present study, we have previously infused calcium gluconate simultaneously with NaH C03 in acute PTX rats in order to prevent the fall in serum calcium, and found that the phos phaturic effect was not diminished [27], Based upon these previous observations, we believe that hypocalcemia cannot account entirely for the present results.…”

Section: Discussionmentioning

confidence: 73%

Relationship between Proximal Tubule Total CO<sub>2</sub> and Phosphate Reabsorption in Acute and Chronic PTX Rats

Kuroda¹,

Aynedjian²,

Zilenovski³

et al. 1978

Kidney Blood Press Res

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The effect of NaHCO₃ infusion on phosphate reabsorption by the proximal convoluted tubule was studied in acute and chronic PTX rats. Either hypertonic NaHCO₃ or NaCl was infused intravenously. Proximal fluid and phosphate reabsorption were measured with ³H-inulin and ³²PO₄, respectively. In acute PTX rats, the fraction of filtered ³²PO₄remaining in the proximal lumen was 5.9% during NaCl infusion and 23% during NaHCO₃infusion (p < 0.001). In the chronic PTX rats, the fraction of filtered ³²PO₄ remaining in the proximal lumen was 24% during NaCl infusion and 38% during NaHCO₂ infusion (p < 0.001). Phosphate reabsorption per unit GFR was reduced by NaHCO₂infusion in both acute and chronic PTX rats. A linear relationship was found between tubular fluid total CO₂ and the fraction of ³²PO₄ remaining in the tubular lumen. The findings indicate that NaHCO₃ infusion inhibits phosphate reabsorption in the proximal convoluted tubule by a mechanism not dependent on PTH or volume expansion, but apparently correlated with intraluminal CO₂.

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Acid-base maneuvers and phosphate transport in the isolated rat kidney

et al. 1981

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The influence of bicarbonate (HCO3-), the carbon dioxide tension (PCO2), and pH on phosphate (Pi) excretion were assessed in isolated rat kidneys, perfused in vitro with recirculating synthetic solutions. After establishing control values, the perfusate HCO3- or PCO2 was altered separately. When the perfusate pH was decreased, either by increasing PCO2 or decreasing HCO3-, the absolute and fractional Pi excretions increased. Perfusate alkalinization by slightly decreasing the PCO2 did not affect Pi excretion, but increasing the perfusate pH with addition of HCO3- elicited phosphaturia. Other kidneys were perfused with a solution from which the CO2/HCO3- buffer system was nominally absent. Alkalinization of HCO3--free perfusate had no effect upon Pi excretion, but acidification resulted in marked phosphaturia. Perfusate acidification, whether achieved by decreasing HCO3-, increasing PCO2, or by adding hydrogen ions, uniformly elicited phosphaturia. The data indicate that either decreasing the extracellular pH or increasing the extracellular HCO3- inhibits renal Pi reabsorption.

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Effect of sodium bicarbonate on phosphate excretion in acute and chronic PTX rats

Cited by 5 publications

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Two‐pore channel protein TPC1 is a determining factor for the adaptation of proximal tubular phosphate handling

Two‐pore channel protein TPC1 is a determining factor for the adaptation of proximal tubular phosphate handling

Relationship between Proximal Tubule Total CO<sub>2</sub> and Phosphate Reabsorption in Acute and Chronic PTX Rats

Acid-base maneuvers and phosphate transport in the isolated rat kidney

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