Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of the light-darkness cycle on the efficiency of the ultimobranchial and parathyroid glands in altering duodenal calcium transport and plasma and urinary concentrations of calcium was examined in the adult male frog (Rana pipiens). Frogs were unfed, but were allowed access to 0.05 M-CaCl2 in the surrounding medium after ultimobranchialectomy or parathyroidectomy. Calcium transport, as assayed by the everted gut-sac technique, was increased in ultimobranchialectomized frogs at sunrise, concomitant with acute hypercalcaemia and hypercalciuria. An opposite but chronic response was observed in parathyroidectomized frogs with intact ultimobranchial glands. The maximum response observed at sunrise occurred when the concentration of calcium in the plasma of control frogs was decreasing; the minimum response, which occurred 6 h after sunrise, was coincident with a diurnal peak in the concentration of calcium. Vitamin D3 (500 microgram/frog) enhanced calcium transport in ultimobranchialectomized frogs, which resulted in chronic hypercalcaemia and hypercalciuria. The results suggest that diurnal variations in the plasma concentration of calcium do not initiate ultimobranchial activity, but are a response to endocrine control synchronized with the transition from darkness to light.
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PMID:Diurnal variations in the influence of the ultimobranchial glands on calcium homeostasis in the frog (Rana pipiens). 21 89

The etiology of hypercalciuria remains unknown in spontaneously hypertensive rats (SHR). In order to differentiate absorptive versus renal hypercalciuria, serial measurements of urinary calcium (UCaV) excretion were made weekly under fasting (3-hour urine collection) and after oral administration of CaCl2 (50 mg/100 g; 4-hour urine collection) from age 8 to 14 weeks in SHR (n = 14) and normotensive Wistar Kyoto rats (WKY; n = 14). Fasting UCaV was significantly greater in WKY than in SHR throughout the periods of observation. In contrast, after oral Ca loading UCaV was greater in SHR after 13 weeks of age (13 weeks: SHR UCaV = 954 micrograms/mg creatinine, WKY UCaV = 541 p less than 0.01; 14 weeks: SHR UCaV = 988 micrograms/mg creatinine, WKY UCaV = 534, p less than 0.01). Fasting urinary cyclic adenosine monophosphate (AMP) excretion was not different between WKY and SHR. However, cyclic AMP excretion of SHR, but not WKY, was decreased after calcium loading when compared to the fasting values. The cyclic AMP was also significantly lower in SHR than in WKY rats after calcium loading. Calcium handling by the kidney was not different between SHR and WKY with or without parathyroidectomy. Calcium disposition kinetic studies were performed on these animals at age 15 and 16 weeks. No significant difference of intravenous 45Ca was observed between WKY (n = 6) and SHR (n = 6) in total plasma clearance, nonrenal clearance, biologic half-life, and elimination rate constant from the central compartment. However, the WKY had a significantly greater renal clearance of 45Ca than the SHR (0.48 +/- 0.04 vs. 0.24 +/- 0.02 ml/n, p less than 0.001). Since tissue disposition of intravenous 45Ca was not different between WKY and SHR, the increased renal excretion of calcium after oral administration in SHR, therefore, reflects increased intestinal absorption of calcium. Correction of established hypertension did not abolish the hypercalciuria. We believe that increased gastrointestinal absorption of calcium is responsible for the hypercalciuria in SHR.
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PMID:Pathogenesis of hypercalciuria in spontaneously hypertensive rats. 396 17

The role of parathyroid hormone (PTH) on calcium excretion during chronic metabolic acidosis was investigated in intact and thyroparathyroidectomized (TPTX) acidotic and control dogs. Intact dogs fed NH4Cl for 3 days developed marked hypercalciuria as compared to intact control animals. After thyroparathyroidectomy, calcium excretion corrected per glomerular filtration rate decreased significantly in NH4Cl-treated dogs but not in the controls. This was observed in the face of a TPTX-induced fall in filtered load of calcium in both groups. After restoration of filtered load of calcium to normal by CaCl2 infusion, fractional calcium excretion at any level of fractional sodium excretion was higher in NH4Cl-treated TPTX dogs than that of TPTX controls, indicating a calciuric effect of acidosis independent of PTH. PtH (1 U/min X 60 min) was infused to examine the effect of this hormone on calcium excretion during NH4Cl-induced acidosis. In normal dogs, PTH significantly decreased absolute and fractional calcium excretion. In contrast, PTH infusion to acidotic dogs failed to decrease absolute and fractional calcium excretion. In both groups, phosphate excretion increased significantly. The higher calcium excretion of acidotic dogs during PTH infusion resulted from failure to enhance calcium reabsorption as shown by the fact that, at any level of plasma ionizable calcium, calcium excretion was higher in acidotic dogs than in controls. These findings indicate that during metabolic acidosis PTH does not exert its normal anticalciuric effect. This may contribute to the development of hypercalciuria despite PTH excess in certain clinical conditions associated with chronic metabolic acidosis.
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PMID:Parathyroid hormone is not anticalciuric during chronic metabolic acidosis. 717 29