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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of NaF, CaCl2, NaCl and mammalian calcitonin on the histology of ultimo-branchial (UTB) and corpuscle of Stannius (CS) and plasma levels of calcium and phosphorus in the teleost Heteropneustes fossilis are recorded. Administration of NaF, NaCl, and mammalian calcitonin resulted in varying degree of hypolcalcaemia and hyperphosphataemia, whereas hypercalcaemia and hypophosphataemia developed during CaCl2 treatment. These treatments also produced various histological changes in UTB and CS. It is suggested that CS and UTB are involved in metabolisms of Ca and P, and in osmoregulation. Moreover, it is an important hypocalcaemic mechanism in this fish in combating hypercalcaemia.
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PMID:Role of ultimobranchial body and corpuscle of Stannius in regulation of the plasma calcium and phosphorus levels in the teleost Heteropneustes fossilis. 103 54

Thirty two specimens of Rana tigrina were divided into four equal groups : group I = controls; group II = injected with Vitamin D2 and placed in a 0.8% aqueous solution of CaCl2; group III = injected with Vitamin D2 and kept in tap water; group IV = placed only in a 0.8% CaCl2 solution. The experimental specimens exhibited varying degrees of hyperactivity of their ultimobranchial gland. Specimens from all the groups were X-rayed. The experimental ones showed different intensity of calcium deposit in their paravertebral lime sacs. The results indicate that prolonged challenge of high calcium induces hyperactivity of the ultimobranchial gland to produce larger quantity of calcitonin, to counteract the experimental hypercalcemia.
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PMID:Effect of a calcium rich environment on the ultimobranchial gland of Rana tigrina. 123 21

The effects of aging on calcitonin (CT) secretion in female rats were investigated. Old (24 mo) at constant diestrus status and young (2 mo) at diestrus status rats were either ovariectomized (Ovx) or left intact as controls. Ovx rats were injected subcutaneously with estradiol benzoate (25 micrograms/kg body wt) or sesame oil one time per day for 3 days. All rats were infused with CaCl2 (10 mg/ml) at a rate of 2 ml/h for 30 min via a jugular catheter connected to a peristaltic pump. Blood samples (0.5 ml each) were collected at 0, 30, 60, and 120 min. The basal and post-CaCl2 levels of plasma Ca measured with radioimmunoassay were significantly higher (P less than 0.05-0.01) in old than in young female rats. The pre- and post-CaCl2 levels of plasma Ca and CT in young rats were not altered by Ovx or estradiol replacement. In old rats, Ovx caused a higher (P less than 0.01) level in plasma CT at 0 and 30 min after CaCl2 infusion. Both basal and stimulated levels of plasma CT were higher (P less than 0.01) in old Ovx than in young Ovx rats. These results demonstrated that 1) the increase of plasma CT in response to Ca challenge was greater in old than in young female rats, 2) the influence of estradiol and ovarian function on plasma CT concentration increases as a function of age, and 3) estradiol reduced the plasma CT in response to hypercalcemia in old Ovx rats. The sensitivity of the target tissue of young rats may be lower in response to the modulation of estrogen during hypercalcemia without compromising the secretion and hypocalcemic effect of CT in young rats. All suggested an age-related relationship between estrogen and CT secretion in minute-to-minute regulation during Ca infusion in rats.
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PMID:Age-related differences in basal and calcium-stimulated plasma calcitonin levels in female rats. 159 Mar 67

Overall 34 patients with terminal renal failure (TRF) and 81 recipients of the allotransplanted cadaveric kidney (ACK) were examined. It has been established in in-vitro experiments with modulated by additions of EDTA to the plasma and CaCl2 hypo- and hypercalcemia that the magnitude of bound calcium (standardized at the concentration of ionized calcium-Ca++1 mmol/l) decreased in the blood plasma in 65 and 61% of cases. Besides protein-bound calcium dropped in 94 and 91% of cases; the total buffer capacity of the plasma and buffer capacity of proteins fell in 59 and 87% of cases in TRF and ACK, respectively. The rise of the Ca++ content on an empty stomach seen in 21 out of 99 patients with TRF and in 42 out of 98 recipients of the ACK was caused by a decrease of calcium binding in the blood plasma, not made for by the fall of calcium supply to the blood because of "tertiary" hyperparathyroidism. Hypocalcemia detected in 38% of TRF patients was consequence to the rise of calcium binding not made for by the increased calcium supply to the blood provoked by bone resistance to parathyroid hormone.
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PMID:[The mechanisms of the disorder of calcium homeostasis in terminal kidney failure and the allotransplantation of a cadaver kidney]. 194 54

Although hypercalcaemia is considered to be aetiological factor of nephrocalcinosis and uroliths formation, its effect on the major salivary glands, where lithiasis is frequent, has not been studied enough. The purpose of this project was the parallel histologic study of the effect of experimentally induced hypercalcaemia on the kidney and the major salivary glands of the rat. Temporary hypercalcaemia was induced in 17 females rates after 8 daily intraperitoneal doses 1.5 ml of 10% calcium gluconate. After the fixation of the tissues in 4% formaldehyde containing 1% CaCl2, serial sections were stained with haematoxylin and eosin and Von Kossa's method for calcified deposits. In the kidneys calcified deposits were observed in the cytoplasm of the cells of the proximal convoluted tubules, in the basement membrane, and their lumen. The major salivary glands were normal. Calcified deposits were not observed in the glandular parenchyma either in the lumina. The results suggest that during hypercalcaemia the transcellular transport of the calcium continue to be under the normal influence of the autonomic nervous system, preventing the formation of calcified deposits.
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PMID:[The effect of the hypercalcaemia on the major salivary glands of the rat]. 194 96

To examine the effects of serum calcium concentrations on PTH biosynthesis, rats were made hyper- (serum total calcium, approximately 3.5 mM) or hypocalcemic (approximately 1.25 mM) and steady-state levels of PTH mRNA in parathyroid cells were measured by the primer extension method using a 32P-labeled synthetic oligomer. PTH mRNA levels increased about twofold in the rats made slightly hypocalcemic by infusion of calcium-free solution and decreased slightly in those made hypercalcemic by CaCl2 infusion (120-150 mumol/h) compared with the levels present in nonfasting control rats. Infusion of calcitonin (0.5 U/h) or EGTA (90 mumol/h) with calcium-free solution increased PTH mRNA levels further (two- to sevenfold) above the levels present in animals infused with calcium-free solution alone. These changes in PTH mRNA levels were observed after 48- but not 24-h infusion, and there was an inverse correlation between PTH mRNA levels and serum calcium concentrations. The results suggest that changes in serum calcium concentrations in the near physiological range regulate the biosynthesis of PTH by affecting steady-state levels of PTH mRNA when hypercalcemia or hypocalcemia continues for a relatively long period.
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PMID:Hypocalcemia increases and hypercalcemia decreases the steady-state level of parathyroid hormone messenger RNA in the rat. 249 84

Chick embryos were injected on the 14th day of incubation with 100 ng calcitriol. The concentration of Ca in their serum rose significantly 4 hours after the injection and the concentration of Pi started to decrease 10 hours after. When embryos of the same age were injected with a solution containing CaCl2, the concentrations of both Ca and P rose significantly 2 hours after the injection and remained high until the end of the experiment. The fact that both treatments produced hypercalcemia but had opposite effects on the concentration of Pi does not agree with the idea that the hypophosphatemic response to calcitriol might be secondary to the hypercalcemia which precedes it. The injection of a solution of NaHCO3 to embryos of the same age failed to produce hypophosphatemia. The fact that calcium salts and bicarbonate, when injected separately, fail to induce hypophosphatemia does not contradict the possibility that the hypophosphatemic response to calcitriol might result from the simultaneous increase in flux of Ca and -HCO3 from the shell. Three days after the injection of calcitriol to 14-day-old embryos, the total amount of Ca and P in the urine was significantly higher than in the controls. The concentration of Ca and P in kidney tissue was also significantly higher in the injected embryos. In addition, calcified precipitates were detected histochemically in the lumen of the kidney tubules from the treated embryos. These results are interpreted as demonstrating that an increase in the excretion of P in the urine is the main mechanism explaining calcitriol-induced hypophosphatemia in the chick embryo.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of calcitriol in phosphate regulation by the chick embryo. 254 19

We examined the calcium contents of desheathed peripheral nerve, perineurial sheath, and whole sciatic nerve in the frog as a function of the steady-state plasma concentration of ionized calcium. Chronic hypocalcemia was induced by parathyroidectomy and by bathing frogs in a phosphate medium. Chronic hypercalcemia was induced by administering vitamin D3 and by bathing frogs for up to 2 wk in medium containing 50 mM CaCl2. Calcium was measured with a calcium-sensitive electrode and by atomic absorption spectroscopy. The calcium contents (mmol/kg wet wt) in whole nerve, desheathed nerve, and the perineurial sheath varied linearly with slopes of 0.72, 0.71, and 1.72, respectively, with plasma concentration (mM) of ionized calcium, which ranged from 0.3 to 8.0 mM. In the same animals the calcium content in the cerebrum was independent of plasma calcium between 0.5 and 1.5 mM but rose at higher plasma concentrations. Our results indicate that net calcium concentration in the frog peripheral nerve is not regulated during chronic hypocalcemia and hypercalcemia, whereas brain calcium is regulated at plasma calcium concentrations less than 1.5 mM. The lack of calcium regulation in the nerve is attributed to the lack of calcium regulation in the endoneurial compartment.
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PMID:Calcium content of frog sciatic nerve during chronic hypocalcemia and hypercalcemia. 282 34

In order to examine the role of calcium in the secretory process of atrial natriuretic factor (ANF), we studied the effects of hypercalcaemia and ouabain on the plasma concentration of immunoreactive ANF, and the effect of calcium on immunoreactive ANF release from isolated rat atria. Anaesthetized dogs were treated with CaCl2 infusion, ouabain or phenylephrine injection. With CaCl2 infusion, serum calcium and plasma immunoreactive ANF respectively increased to three and four times their basal levels. Ouabain increased plasma immunoreactive ANF to two and a half times the initial level. Neither CaCl2 nor ouabain produced any effect on right atrial pressure and heart rate, but they both significantly increased arterial pressure. Phenylephrine caused a greater increase in arterial pressure than both CaCl2 and ouabain. However, there was no significant increase in plasma immunoreactive ANF. Moreover, calcium stimulated the release of immunoreactive ANF from isolated rat atria. These results suggest that the calcium may play a key role in the secretory process of ANF.
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PMID:Effects of calcium and ouabain on the release of atrial natriuretic factor. 297 69

Studies were designed to investigate the potential importance of calmodulin in release of calcitonin (CT) in response to an increase in the concentration of extracellular Ca. In vitro release of CT from baby rat thyroparathyroids incubated up to 8 h was examined at normal (1 mM) and high (2.5 mM) Ca in serum-free medium in the presence and absence of the potent calmodulin inhibitors, trifluoperazine (TFP) and N-(6-aminohexyl)-5-Cl-1-naphthalene sulfonamide (W-7). The drugs chlorpromazine (CLP) and haloperidol (HAL) which, like TFP, are anti-psychotic agents also were tested. In some studies release of parathyroid hormone (PTH) into medium also was studied. At 2.5 mM Ca, CT release was increased five- tenfold compared with 1 mM Ca while PTH was suppressed by approximately 80%. The increased release of CT induced by 2.5 mM Ca was inhibited 60-90% by 10(-4) M TFP and 10(-4) M W-7, but was unaffected by 10(-4) M CLP or HAL. In the presence of 1 mM Ca, the increased release of PTH also was inhibited significantly by 10(-4) M TFP and 10(-4) M W-7. In related in vivo studies, administration of TFP i.v. to rats just before induction of hypercalcemia with i.v. CaCl2 suppressed the increase in plasma CT normally observed 3 min later in a dose-related manner. The results show that calmodulin inhibitors can inhibit in vitro secretion of CT, and release of PTH as well. Additionally, inhibition of the in vivo CT response to a Ca challenge was observed within minutes of drug administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of secretion of rat calcitonin by calmodulin inhibitors. 308 92


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