|
pubmed:abstractText |
With hyperparathyroidism, serum bicarbonate (HCO(3) (-)) is low, urinary excretion of HCO(3) (-) is increased and the apparent T(m) for HCO(3) (-) is reduced. These findings have been ascribed to a direct renal action of parathyroid hormone (PTH). Since hypophosphatemia and phosphate depletion may occur in hyperparathyroidism, it is possible that phosphate depletion could account for the abnormal renal HCO(3) (-) handling. To test this possibility, renal reabsorption of HCO(3) (-) was evaluated in dogs before and after phosphate depletion. Serum HCO(3) (-) was significantly lower in phosphate depleted dogs than in normal animals, and serum HCO(3) (-) was directly related to serum phosphorus. Both the threshold at which HCO(3) (-) appeared in the urine and the T(m) for HCO(3) (-) were reduced during phosphate depletion. Intracellular pH of muscle was significantly higher in phosphate depleted dogs than in normals and the pH returned to normal after phosphate repletion. These data show that phosphate depleted dogs, which probably have physiological hypoparathyroidism, display abnormalities in both serum HCO(3) (-) and its renal handling which are similar to those seen in hyperparathyroidism, supporting the concept that the PTH-induced alterations in HCO(3) (-) homeostasis may be due to phosphate depletion. The latter could alter cell metabolism, resulting in reduced intracellular H(+) concentration, which may then impair H(+) secretion by the renal tubules and decrease their ability to reabsorb HCO(3) (-). Consequently, T(m) HCO(3) (-) and serum HCO(3) (-) fall.
|
