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)

Hypercalciuria has been reported in rats with mild hyperprolactinemia due to implantation of anterior pituitary glands under the kidney capsule and in rats bearing transplantable tumors that secrete large amounts of prolactin (PRL) and growth hormone (GH). We studied Buffalo rats implanted subcutaneously with the new MMQ pituitary tumor line that secretes only PRL. Urinary calcium excretion increased as the tumors grew. Three weeks after tumor implantation in female rats, the urinary calcium excretion was 1.102 +/- 0.092 mg/100 g body weight (BW).24 hours compared with controls, 0.296 +/- 0.079, P less than .0005. Male tumor-bearing rats also had increased urinary calcium excretion compared with male controls. In tumor-bearing rats the urinary calcium excretion factored for urinary sodium excretion, dietary calcium intake, or urinary creatinine excretion was elevated. Urinary calcium excretion was correlated with serum PRL levels and with estimated tumor volume. Serum calcium, immunoassayable parathyroid hormone, and urinary cyclic adenosine monophosphate (cAMP) excretion were normal in the tumor-bearing rats. There was some evidence of loss of bone calcium in rats bearing the MMQ tumor, and serum levels of calcitonin were decreased. These results are similar to those found in anterior pituitary-grafted hypercalciuric rats. It is unlikely that parathyroid hormone (PTH) abnormalities are responsible for the hypercalciuria in the MMQ-bearing rats. The pituitary gland may have an effect on the distal renal tubule to decrease calcium reabsorption.
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PMID:Hypercalciuria in a new rat model of hyperprolactinemia. 184 86

The anterior pituitary (AP) grafted, adrenalectomized, steroid hormone-replaced male rat is characterized by hyperprolactinemia and hypercalciuria. To determine the origin of the hypercalciuria, clearance experiments were performed under Inactin anesthesia in adrenalectomized Fischer rats 8-10 wk after implantation of extra AP glands under the kidney capsule. Glomerular filtration rate, ultrafilterable calcium, and fractional sodium excretion were comparable in the AP and control groups. However, fractional calcium excretion was significantly higher in the AP-implanted rats, P less than 0.05, resulting in a marked dissociation of the calcium/sodium clearance ratio. Because filtered calcium load did not change, these results clearly demonstrate that AP-implanted animals have a defect in tubular calcium reabsorption. The dissociation of calcium transport from sodium transport suggests the distal tubule as a likely site of action. Parathyroidectomy did not alter the calciuric response to AP implantation. To test whether hyperprolactinemia was responsible for decreased calcium reabsorption in AP-implanted rats, purified rat prolactin was infused into normal rats to achieve high blood prolactin levels, or was injected into normal rats daily for 8 days. Changes in fractional calcium excretion and the ratio of calcium to sodium clearance were identical in animals receiving prolactin or control infusions. Thus, hypercalciuria in the AP-implanted rat may be attributed to an unidentified factor, perhaps secreted from the implanted anterior pituitaries, rather than to prolactin excess.
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PMID:Examination of hypercalciuria in anterior pituitary-implanted rats. 357 34

There is evidence that prolactin (PRL) excess plays a role in the etiology of osteoporosis associated with human prolactinoma. Calcium balance in human hyperprolactinemia has not been thoroughly investigated. In the present study, rats with excess circulating PRL levels (male anterior pituitary-grafted Fischer 344 rats) had urinary calcium excretion twice that of control rats (4.16 +/- 0.43 v 2.25 +/- 0.30 mg/24h X 100 g BW). Calcium excretion expressed per mg of calcium intake was also high in pituitary-grafted rats. The excess calcium excretion in hyperprolactinemic rats was not accompanied by a concomitant rise in sodium excretion. This dissociation suggests that PRL has an effect on the renal handling of calcium. Since thiazide diuretics have a well-described hypocalciuric action, their effect was tested in these rats. In normal rats, benzthiazide, a long-acting agent, significantly reduced urinary calcium excretion in a dose-dependent fashion. Hyperprolactinemic rats responded to benzthiazide in a manner similar to control rats. In pituitary-grafted rats, benzthiazide also decreased the calcium excretion to intake ratio and normalized the calcium to sodium excretion ratio. Since the hypercalciuria of experimental hyperprolactinemia can be corrected by thiazide diuretics, these agents may have therapeutic potential in human PRL excess.
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PMID:Hypercalciuria in hyperprolactinemic rats: effects of benzthiazide. 372 59

A study was made into the structural-and-functional status of the osseous tissue in patients with neuroendocrinemetabolic form of the hypothealamic syndrome. Noted in the above patients were abnormalities in the calcium-phosphorous balance which are manifested by a drop in the blood level of calcium and by profound hypercalciuria. All examinees have been shown to present with the osteopenic syndrome formation. Possible causes of development of systemic osteopenia in those patients presenting with neuroendocrinemetabolic form of the hypothalamic syndrome are believed to include, in the first place, hypercorticoidism, hyperprolactinemia, reduction in the estrogen secretion, which might be result in imbalance of processes of bone remodelling involving largely resorption of the bone.
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PMID:[State of osseous tissue in patients with the neuroendocrine metabolic form of hypothalamic syndrome]. 1271 13