Effects and interrelationships of PTH, Ca2+, vitamin D, and Pi in acid-base homeostasis
| Autor: | H. N. Hulter |
|---|---|
| Rok vydání: | 1985 |
| Předmět: |
medicine.medical_specialty
Sodium-Hydrogen Exchangers Physiology Urinary Bladder Metabolic alkalosis Acid–base homeostasis Kidney Epithelium Phosphates Parathyroid Glands Calcitriol Internal medicine Hyperchloremic acidosis medicine Animals Humans Vitamin D Egtazic Acid Calcifediol Acidosis Acid-Base Equilibrium Hyperparathyroidism Chemistry Alkalosis Nephrons medicine.disease Bicarbonates Kidney Tubules Endocrinology medicine.anatomical_structure Parathyroid Hormone Thyroidectomy Calcium Hyperparathyroidism Secondary medicine.symptom Carrier Proteins Hypophosphatemia Homeostasis Glomerular Filtration Rate |
| Zdroj: | American Journal of Physiology-Renal Physiology. 248:F739-F752 |
| ISSN: | 1522-1466 1931-857X |
| Popis: | Chronic administration of 1,25(OH)2D or PTH increases the set point at which plasma bicarbonate concentration is regulated by the kidney and thereby maintains metabolic alkalosis in a variety of species. The renal mechanism(s) responsible for the chronic acid excretory response to 1,25(OH)2D and PTH administration have not been defined, but indirect evidence suggests effects on distal nephron segments. With either hormone in dogs, but not in rats, metabolic alkalosis is generated in part by extrarenal mechanisms. Contrary to the variable finding of hyperchloremic acidosis in human primary hyperparathyroidism, a steady state of mild metabolic alkalosis of renal origin is achieved in normal human subjects infused chronically with PTH. The multiple potential mechanisms responsible for this discrepancy will require careful consideration in future investigations. The acute and chronic effects of plasma calcium concentration on both renal and extrarenal acid-base homeostasis are incompletely understood and require extensive further investigation. Studies in rats have suggested that phosphate depletion results in important counterbalancing renal acidosis and extrarenal alkalosis-producing effects. Chronic hypophosphaturia in the absence of appreciable hypophosphatemia can also result in impaired renal acidification by virtue of phosphate's property as a luminal buffer. |
| Databáze: | OpenAIRE |
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