Effects of Chlorothiazide Administration and Dietary Calcium Restriction on Parathyroid Function, Vitamin D Metabolism and Intestinal Calcium Absorption in the Rat
Thiazide diuretic agents reduce urine calcium excretion by stimulating distal nephron calcium reabsorption and by reducing extracellular fluid volume (1–3). In patients with idiopathic hy-percalciuria, thiazide administration lowers urinary calcium excretion. In addition, circulating 1,25(OH)2D3 and intestinal calcium absorption rates can also be reduced to normal in those patients with hypercalciuria arising from defective tubular calcium reabsorption (4, 5). Its effects upon serum 1,25(OH)2D3 and intestinal calcium absorption could be due to the reversal of secondary hyperparathyroidism (6). The physiological adaptation to dietary calcium restriction involves an increase in 1,25(OH)2D3 synthesis which, in turn, enhances the intestinal calcium active transport process (7–9). Since this sequence of events is thought to be initiated by an increase in parathyroid hormone (PTH) secretion, we investigated whether thiazide can prevent the intestinal adaptive response to low calcium diet (LCD).
KeywordsSecondary Hyperparathyroidism Intestinal Calcium Absorption Idiopathic Hypercalciuria Increase Calcium Uptake Immunoreactive Parathyroid Hormone
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