Acute metabolic acidosis enhances circulating parathyroid hormone, which contributes to the renal response against acidosis in the rat.

@article{Bichara1990AcuteMA,
  title={Acute metabolic acidosis enhances circulating parathyroid hormone, which contributes to the renal response against acidosis in the rat.},
  author={Maurice Bichara and Olaf Mercier and Pascale Borensztein and Michel Paillard},
  journal={The Journal of clinical investigation},
  year={1990},
  volume={86 2},
  pages={
          430-43
        }
}
Acute PTH administration enhances final urine acidification in the rat. HCl was infused during 3 h in rats to determine the parathyroid and renal responses to acute metabolic acidosis. Serum immunoreactive PTH (iPTH) concentration significantly increased and nephrogenous adenosine 3H,5H-cyclic monophosphate tended to increase during HCl loading in intact and adrenalectomized (ADX) rats despite significant increments in plasma ionized calcium. Strong linear relationships existed between serum… 
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Direct Effect of Acute Metabolic and Respiratory Acidosis on Parathyroid Hormone Secretion in the Dog
TLDR
It is concluded that acute Met Acid acts as a secretogogue for PTH secretion because it enhances the maximal PTH response to hypocalcemia and EDTA was infused to prevent acidosis‐induced increases in ionized calcium.
Acute variations in extracellular pH modulate transduction pathways of PTH in rat proximal tubule.
TLDR
Variations in pHe, which induced parallel variations in intracellular pH (pHi), did not affect unstimulated values for adenosine 3',5'-cyclic monophosphate (cAMP) production, inositol trisphosphate accumulation, or cytosolic free Ca2+ concentration, while variations in pHi may affect per se adenylyl cyclase activity.
Chronic metabolic acidosis increases the serum concentration of 1,25-dihydroxyvitamin D in humans by stimulating its production rate. Critical role of acidosis-induced renal hypophosphatemia.
TLDR
In conclusion, metabolic acidosis results in graded increases in serum 1,25-(OH)2D concentration by stimulating its production rate in humans, which is explained by acidosis-induced hypophosphatemia/cellular phosphate depletion resulting at least in part from decreased renal tubular phosphate re absorption.
Direct Effect of the Correction of Acidosis on Plasma Parathyroid Hormone Concentrations, Calcium and Phosphate in Hemodialysis Patients: A Prospective Study
TLDR
This study demonstrates that the correction of metabolic acidosis in chronic HD patients reduces iPTH concentrations in HD patients with secondary hyperparathyroidism possibly by a direct effect on iPTH secretion.
Correction of acidosis in hemodialysis patients increases the sensitivity of the parathyroid glands to calcium.
TLDR
The correction of metabolic acidosis in hemodialysis patients with secondary hyperparathyroidism can suppressParathyroid hormone secretion by increasing the sensitivity of the parathyroid glands to ionized calcium.
Pathophysiologic Changes in Extracellular pH Modulate Parathyroid Calcium-Sensing Receptor Activity and Secretion via a Histidine-Independent Mechanism.
TLDR
It is suggested that acid-base disturbances may affect the CaR-mediated control of parathyroid function and calcium metabolism in vivo.
Molecular mechanisms and regulation of urinary acidification.
  • I. Kurtz
  • Biology, Medicine
    Comprehensive Physiology
  • 2014
TLDR
A broad review of a field that began historically ~60 years ago with whole animal studies, and has evolved to where it is currently addressing questions related to kidney acid-base regulation at the single protein structure/function level is provided.
Chronic metabolic acidosis in azotemic rats on a high-phosphate diet halts the progression of renal disease.
TLDR
The presence of chronic metabolic acidosis in 5/6 nephrectomized rats on a high-phosphate diet protected against the progression of RF, enhanced the renal clearance of phosphate, resulted in a lesser degree of hyperparathyroidism, and did not reduce the osteoblast surface.
Renal and Skeletal Actions of Parathyroid Hormone (PTH) and PTH-Related Protein
Phosphorus and protein restriction and parathyroid function in chronic renal failure.
TLDR
A direct inhibition of PTH secretion over a wide range of iCa concentration by LPD in patients with advanced CRF and mild HPT II over a three months period is demonstrated, independent of changes in plasma calcitriol levels.
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References

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TLDR
The results indicate that chronic acidosis elevates iPTH mainly by producing hypercalciuria and that acidosis itself is not a primary stimulus to PTH secretion.
Effects of antidiuretic hormone on urinary acidification and on tubular handling of bicarbonate in the rat.
TLDR
It is concluded that antidiuretic hormone (ADH) inhibits fractional bicarbonate absorption in the thick ascending limb while stimulating that of chloride at least in TPTX somatostatin-infused rats, and ADH stimulates proton secretion in the distal tubule and cortical collecting ducts, which leads to enhanced urinary acidification.
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TLDR
The results indicate that PTH is necessary for the optimal buffering of large, acute acid loads presumably by increasing bone buffering, supported by the observation that P TH did not alter the pH of intact rat diaphragms in vitro.
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TLDR
Measurements of urinary ammonium and titratable acid indicate that net acid excretion increases significantly after PTH administration, consistent with the view that PTH inhibits proximal tubular HCO-/3 reabsorption with normal or high filtered loads of HCO/3, but distal segments of the nephron are able to reabsorb the excess delivered from the proximaltubule.
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TLDR
It is concluded that PTH stimulates collecting duct H+ secretion indirectly via the increase in [Pi]u, which is higher for any value of urinary bicarbonate concentration in the presence of PTH and urinary phosphate concentration in its absence.
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TLDR
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TLDR
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TLDR
The data are interpreted to support the hypothesis that neither PTH nor vitamin D and its metabolites mediates the increase in net bone resorption that must accompany chronic metabolic acidosis.
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TLDR
The acidification defect in this model of SAD appears to be a result of a decrease in ammonia production and delivery to the loop of Henle, impaired transfer from loop to collecting duct and reduction in the rate of H+ secretion by the collecting duct.
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  • Biology, Medicine
    The American journal of physiology
  • 1985
TLDR
The data suggest that acid-base balance may modulate tubular phosphate transport independent of intraluminal pH and phosphate concentration, and these changes depend on the chronicity of exposure and act independent but integral to the effects of parathyroid hormone and the intrinsic adaptation to dietary phosphate availability.
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