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ACUTE LITHIUM ADMINISTRATION IMPAIRS THE ACTION OF PARATHYROID HORMONE ON RAT RENAL CALCIUM, MAGNESIUM AND PHOSPHATE TRANSPORT *
Author(s) -
Carney Shane,
Jackson Peggy
Publication year - 1998
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1998.tb02155.x
Subject(s) - parathyroid hormone , endocrinology , chemistry , medicine , excretion , reabsorption , calcium , sodium , lithium (medication) , parathyroidectomy , phosphate , kidney , biochemistry , organic chemistry
SUMMARY 1. Chronic lithium (Li + ) treatment commonly produces a state of hyperparathyroidism in humans and rat although the mechanism is unknown. 2. The present study evaluated the acute effect of Li + on renal electrolyte transport, particularly Ca 2+ and Mg 2+ in thyroparathyroidectomized (TPTX) and intact rats. 3. The acute administration of Li + significantly increased water, sodium, potassium and phosphate excretion in both TPTX and intact animals; however, Ca 2+ and Mg 2+ excretion was only increased in the intact group. Fractional excretion (FE) of Ca 2+ and Mg 2+ increased from 2.2±0.2 to 3.5±0.3% and 12±2 to 18±2%, respectively ( P <0.01). 4. In further experiments in TPTX rats, Li + administration inhibited the usual reduction in urine Ca 2+ and Mg 2+ excretion following parathyroid hormone (PTH) administration and inhibited the phosphaturia. However, supramaximal concentrations of PTH overcame this inhibitory effect. For example, an FE Ca of 3.8±0.2% was reduced to 1.4±0.2% and 1.7±0.2% with maximal and supramaximal PTH concentrations, respectively, while in the presence of Li + an FE ca of 4.0±0.2 was decreased to 2.8±0.2 and then 1.9±0.3% with the same PTH concentrations. 5. The inhibitory effect of Li + was reduced with a lower plasma Li + concentration (0.7±0.2 vs 1.6–1.8 mmol/L). The FE Mg results were comparable. 6. These results demonstrate that Li + directly inhibits PTH‐mediated renal reabsorption of Ca 2+ and Mg 2+ and also blunts PTH‐mediated phosphaturia. Therefore, the hyperparathyroidism in humans following Li + treatment may be a consequence of reduced renal Ca 2+ reabsorption.