Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experiments were designed to study the rapidity of changes in plasma 1,25-dihydroxyvitamin D [1,25-(OH)2D] levels in response to hypercalcemia and hypocalcemia induced by 10-h infusions of CaCl2 or EGTA in steers. In response to CaCl2 infusions, 1,25-(OH)2D was decreased within 4 h (P less than 0.05) and remained lower (P less than 0.05) than preinfusion concentrations for up to 14 h after termination of the infusions. PTH and inorganic phosphate (Pin) transiently decreased in response to the CaCl2 infusions, whereas total magnesium (Mg) continuously fell for up to 24 h after the start of the infusions. In response to infusions with EGTA, on the other hand, 1,25-(OH)2D continuously increased and was raised significantly (P less than 0.05) between 12 and 24 h after the start of the infusions. PTH increased within 2 h (P less than 0.05) and remained elevated (P less than 0.05) for up to 2 h after the end of the EGTA infusions, whereas Pin and Mg were not significantly changed. During and after 10-h control infusions of sodium chloride, the levels of 1,25-(OH)2D, PTH, Ca, Ca++, Pin, and Mg remained unaltered. In conclusion, plasma levels of 1,25-(OH)2D were lowered in response to hypercalcemia within 4 h and increased in response to hypocalcemia within 12 h. After termination of the infusions with CaCl2 or EGTA, levels of 1,25-(OH)2D remained decreased or elevated for at least 14 h, even though Ca, Ca++, and PTH levels were normalized. The slow changes in 1,25-(OH)2D contrast with the rapid responses of PTH to hyper- and hypocalcemia.
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PMID:Rapidity of plasma 1,25-dihydroxyvitamin D responses to hypo- and hypercalcemia in steers. 640 84

The hypocalcemic effect of gastrin and its possible mode of action were studied in rats. Gastrin (13 micrograms/100 g rat), injected intravenously led to a significant reduction in the plasma calcium concentrations. The release of endogenous gastrin by an intragastric phenylalanine instillation similarly led to a significant hypocalcemia in intact rat but not in antrectomized rat. Moreover, the protective role of endogenous gastrin against hypercalcemia induced by an intraduodenal infusion of CaCl2 (10 mg/100 g rat) was demonstrated. Gastrin (50 microgram/100 g rat) seems to have no influence on the net intestinal absorption of 45Ca. The removal of 45Ca from plasma was also unaffected by gastrin administration. The disappearance rate from plasma of 45Ca administered 17 hr previously was compared in sham, thyroidectomized (TX) and parathyroid-autotransplanted rats receiving saline or gastrin. The faster rate of disappearance of plasma 45Ca from plasma in gastrin-treated TX autoparathyroid-transplanted rats indicated the suppressive action of gastrin on the release of 45Ca from as yet unknown source(s).
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PMID:Possible role and mode of action of gastrin on calcium homeostasis in the rat. 732 69

Hypercalcemia causes acute pancreatitis in humans, a phenomenon reproduced experimentally in cats and guinea pigs. Because the rat is the most frequently used animal for the study of experimental pancreatitis, the present studies were performed to evaluate the effects of hypercalcemia in the rat. In in vitro studies, pancreatic lobules were prepared from fasted Wistar rats (200-250 g) and incubated in HEPES bicarbonate-buffered medium (pH 7.4) containing 0, 0.6, 1.2, 2.5, 5, and 10 mM CaCl2 with or without carbachol 10(-6) M. Amylase was measured in the medium after 30 min to 3 h, and expressed as percent of total amylase. In in vivo studies, fasted male Wistar rats (300-400 g) received calcium (CaCl2; 0.6 mmol/kgh) into the tail vein for 12 h. Control animals received NaCl 0.9% infusion. Histologic slides (H&E-stained) were evaluated in a blinded fashion. Pancreatic lobules showed a higher basal amylase output when incubated in higher calcium medium. The largest, significant difference (2.6-fold) was between 0.6 and 5 mM medium CaCl2 (p < 0.05). Carbachol-stimulated amylase release was again higher with increasing medium calcium with the most pronounced difference (1.3-fold) between 0.6 and 2.5 mM CaCl2 (p < 0.05). In vivo calcium-treated animals showed accumulation of zymogen granules in the cytoplasm, cytoplasmic vacuolization, focal acinar cell depolarization, acinar necrosis, and edema. Calcium causes amylase release from rat pancreatic lobules in vitro. Higher medium calcium levels both significantly increase amylase release from unstimulated and carbachol stimulated lobules. Twelve-hour in vivo calcium infusion leads to accumulation of zymogen granules in acinar cells and acinar injury.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A rat model to study hypercalcemia-induced acute pancreatitis. 752 Sep 26

The local surgical manipulation of sympathetic and parasympathetic nerves innervating the thyroid-parathyroid territory was employed to search for the existence of a peripheral neuroendocrine link controlling parathyroid hormone (PTH) and calcitonin (CT) release. From 8 to 24 h after superior cervical ganglionectomy (SCGx), at the time of wallerian degeneration of thyroid-parathyroid sympathetic nerve terminals, an alpha-adrenergic inhibition, together with a minor beta-adrenergic stimulation, of hypercalcemia-induced CT release, and an alpha-adrenoceptor inhibition of hypocalcemia-induced PTH release were found. In chronically SCGx rats PTH response to EDTA was slower, and after CaCl2 injection, serum calcium attained higher levels in face of normal CT levels. SCGx blocked the PTH increase found in sham-operated rats stressed by a subcutaneous injection of turpentine oil, but did not affect the greater response to EDTA. The higher hypocalcemia seen after turpentine oil was no longer observed in SCGx rats. The effects of turpentine oil stress on calcium and CT responses to a bolus injection of CaCl2 persisted in rats subjected to SCGx 14 days earlier. Interruption of thyroid-parathyroid parasympathetic input conveyed by the thyroid nerves (TN) and the inferior laryngeal nerves (ILN) caused a fall in total serum calcium, an increase of PTH levels and a decrease of CT levels, when measured 10 days after surgery. Greater responses of serum CT and PTH were detected in TN-sectioned, and in TN- or ILN-sectioned rats, respectively. Physiological concentrations of CT decreased, and those of PTH increased, in vitro cholinergic activity in rat SCG, measured as specific choline uptake, and acetylcholine synthesis and release. The results indicate that cervical autonomic nerves constitute a pathway through which the brain modulates calcium homeostasis.
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PMID:Influence of the autonomic nervous system on calcium homeostasis in the rat. 792 Sep 72

The present data reveal that (a) the Stannius corpuscles (CS) of Ompok bimaculatus are active even in their natural freshwater environment (0.4 mM Ca2+/liter) and produce hypocalcemic hormone or stanniocalcin, which lowers the Ca level in normal freshwater fish injected with 0.2 ml of CS extract (1 mg of CS) per fish, (b) this hypocalcemic activity is enhanced in fish that are adapted to a calcium-rich environment (0.6% CaCl2 solution), and (c) adaptation to this calcium-rich environment leads to hypercalcemia in fish. Administration of the extract (from fish previously reared in 0.6% CaCl2 medium) to hypercalcemic fish leads to severe hypocalcemic conditions. It is suggested that the CS of O. bimaculatus produce a general hypocalcemic hormone which is active in the natural freshwater environment (with 0.4 mM Ca2+/liter) and whose activity is enhanced under hypercalcemic conditions after adaptation to a calcium-rich habitat.
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PMID:Evidence for general hypocalcemic hormone from the stannius corpuscles of the freshwater catfish Ompok bimaculatus (Bl). 792 28

An in vivo whole animal 45Ca influx bioassay was used to study the cholinergic control of the release of stanniocalcin (STC) in the rainbow trout (Oncorhynchus mykiss) and the American eel (Anguilla rostrata). In both species calcium influx (JinCa2+) was lowered in response to hypercalcemia induced by intravascular (trout) or intraperitoneal (eel) injections of CaCl2. In trout, this response was blocked by the cholinergic antagonist atropine (0.25 mumol kg-1) and mimicked by the cholinoceptor agonist carbachol (0.25 mumol kg-1). These observations are consistent with a cholinergic stimulation of STC release in response to hypercalcemia in trout. In eels, pretreatment with atropine did not block the lowering of JinCa2+ in response to hypercalcemia. This suggests that cholinergic stimulation is not obligatory for stanniocalcin release in eels. However, carbachol treatment did elicit STC release as revealed by the lowering of JinCa2+. This response to carbachol was not observed in stanniectomized eels. Thus, in the American eel it appears that there is a potential for cholinergic control of STC release but that other factors such as the local plasma calcium concentration may also be involved, at least in response to severe acute hypercalcemia.
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PMID:Cholinergic control of stanniocalcin release in the rainbow trout, Oncorhynchus mykiss, and the American eel, Anguilla rostrata. 804 58

This study analyzes the parathyroid function in four dogs before and after 2 years of a low-calcium, high-sodium, vitamin D-deficient diet and the involution of the same function following (1) correction of dietary calcium deficiency and administration of i.v. 1,25-(OH)2D (0.25 micrograms twice per day) during 1 month, (2) after an additional month of normal dog chow supplemented with oral vitamin D (25 micrograms per day), and, finally, (3) after 5 and 17 months of a diet with normal levels of calcium and vitamin D. The parathyroid function was evaluated through i.v. infusion of CaCl2 and Na2 EDTA with measurement of intact (I) and carboxyl-terminal (C) immunoreactive parathyroid hormone (iPTH). The C-iPTH/I-iPTH ratio was calculated to assess the modulation of molecular forms of iPTH induced by the various treatments. The 2 years of calcium and vitamin D deprivation lowered ionized calcium (1.23 +/- 0.04, p < 0.05) and 25-OHD (4.02 +/- 2.06 nM, p < 0.005) and tended to decrease 1,25-(OH)2D (80.8 +/- 8.6 pM); it increased basal I- and C-iPTH levels approximately eightfold (I-iPTH, 40.2 +/- 20.7, p < 0.05; C-iPTH, 185.4 +/- 94.9, p < 0.05) and stimulated I-iPTH (60.2 +/- 23.0 pM, p < 0.05) and C-iPTH (239.6 +/- 80.7 pM, p < 0.05) fivefold. A greater rise in nonsuppressible I-iPTH levels than in C-iPTH levels led to a decreased C-iPTH/I-iPTH ratio in hypercalcemia (12.5 +/- 2.8 versus 27.8 +/- 6.05 pM, p < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lack of involution of hyperplastic parathyroid glands in dogs: adaptation via a decrease in the calcium stimulation set point and a change in secretion profile. 805 90

The effects of acute hypercalcemia on renal function were evaluated in anesthetized mongrel dogs. Calcium concentration was increased by infusion of CaCl2 solution into the left renal artery at two different rates. At the lower rate of infusion (0.010 mM/kg/min) the plasma total calcium concentration in the left kidney increased from 2.5 mM/l to 3.76 mM/l and the arterial plasma total calcium concentration to 2.94 mM/l. Renal vascular resistance in the left kidney did not change in association with a small decrement in the renal blood flow (9.5%). The glomerular filtration rate decreased from 82.9 ml/min to 65.9 ml/min in association with a small decrease in the urine output. The calcium excretion increased slightly from 3.3 microM/min to 4.05 microM/min. When this amount of CaCl2 was infused into the left renal artery the parameters of the right intact kidney did not change. During the higher rate of infusion (0.020 mM/kg/min) in the left kidney the plasma total calcium concentration in the left kidney increased from 2.3 mM/l to 6.15 mM/l and in the arterial plasma to 3.4 mM/l. Renal vascular resistance increased considerably from 1.66 to 4.0 and the renal blood flow decreased from 482 ml/min to 311 ml/min. The glomerular filtration rate dropped from 78.7 ml/min to 43 ml/min with a significant decrease in the urine output. The calcium excretion increased from 4.35 microM/min to 7.5 microM/min. In the right kidney during the CaCl2 infusion the CPAH decreased from 304 ml/min to 239 ml/min showing that there was an increase in the vascular resistance in association with decrements in Cinulin from 85 ml/min to 67.2 ml/min. These data prove a direct, but not linear relationship between the total plasma calcium concentration and the renal vascular resistance. We suppose that the distal tubular calcium load participates in the distal tubular feedback regulation, when the calcium ion concentration in the tubular fluid at the macula densa increases. This increment elicits vasoconstriction in the afferent arteriole decreasing the filtered calcium load in the glomeruli.
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PMID:Effects of hypercalcemia on kidney function in anesthetized dogs. 806 52

Calcium concentration of pancreatic juice depends on secretion of calcium bound to enzymatic proteins or calcium diffusion from interstitial fluids. To evaluate the relative magnitude of these pathways, we studied the influence of hypercalcemia on ionized calcium (Ca++) in dog pancreatic juice. Pancreatic juice was collected during basal secretion and during stimulation by secretin or secretin plus caerulein in control conditions and under CaCl2 infusion. [Ca++] was measured by selective electrodes. Saturation of juice in CaCO3 was calculated. In stimulated juice, total calcium concentration ([CaT]) and [Ca++] were unchanged by hypercalcemia. In basal juice, composition was profoundly modified by hypercalcemia because [CaT] (3.31 +/- 0.89 mmol/L vs 1.80 +/- 0.44 for controls), [Ca++] (1.44 +/- 0.37 mmol/L vs 0.84 +/- 0.24 mmol/L for controls), and the index of saturation in CaCO3 (5.2 +/- 2.4 vs 2.9 +/- 1.8 for controls) increased significantly. Protein concentration was unchanged. This suggests that in basal conditions, the relationship between plasma and juice calcium levels is due to passive interstitial Ca++ diffusion through the pancreatic ducts. In accordance with the hypothesis of a restricted calcium diffusion, the effects of hypercalcemia were flow rate dependent, being less pronounced when basal flow rate increased. It is concluded that, in the dog, the calcium species found in stimulated juice result from a redistribution of calcium secreted along with proteins, whereas at low secretion rate, juice calcium level depends mainly on interstitial Ca++ diffusion into the main pancreatic ducts.
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PMID:Influence of hypercalcemia on ionized calcium concentration in pancreatic juice of the dog. 814 5

To outline the role of post-translational events in the control of the parathyroid function in vivo, we have studied the parathyroid function of normal dogs receiving i.v. infusions of CaCl2 and Na2EDTA with intact (I), carboxylterminal (C) and midcarboxylterminal (M) iPTH assays and evaluated the influence of ionized calcium on circulating molecular forms of iPTH via alterations in C/I, M/I and M/C iPTH ratios. Furthermore, the use of the mathematical model fitting the sigmoidal relationship between ionized calcium and iPTH ratios was improved through the generation of more iPTH ratio points in the ascending part of the sigmoid function. Quantitatively, the response to hypocalcemia was highest with M (98.7 +/- 36.8 pmol/l; P < 0.0167 vs. L and P < 0.0001 vs. I) and higher with L (83.1 +/- 26.1 pmol/l; P < 0.0001 vs. I) than with I (12.1 +/- 3.2 pmol/l). Similar results were observed for the non-suppressible fraction of iPTH measured by the three iPTH assays in hypercalcemia. The slope of the sigmoid function was more acute for I than for C or M, while all three secretion set-points were similar at 1.30 mmol/l. Qualitatively, all iPTH ratios increased from hypo- to hypercalcemia, results being more pronounced for the M/I and C/I iPTH ratios (7.66 +/- 2.57 to 73.9 +/- 41.4 and 6.76 +/- 1.93 to 49.8 +/- 27.5) than for the M/C iPTH ratio (1.24 +/- 0.48 to 1.82 +/- 1.16). The slopes of the three ratios were similar as were the set-points, but in this last case, values were higher (1.40 mmol/l) than for secretion set-points. These results indicate that dog parathyroid function is similar to that of man. The lower set-points for secretion and higher ones for regulating M/I and C/I iPTH ratios favor an optimal amount of I in face of decreasing ionized calcium and permit to control the non-suppressible fraction of iPTH secretion via M and C fragments production in face of increasing ionized calcium. These events are important to understand the implication and signification of post-translational events in the parathyroid glands and in peripheral blood in the phenomenon of PTH immunoheterogeneity. They further outline that the tools used here will be useful to study similar phenomenons in individuals in face of diseased parathyroid glands.
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PMID:Immunological evidences for post-translational control of the parathyroid function by ionized calcium in dogs. 826 53


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