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Results for “Calcium homeostasis”

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At least 19 recordsLinked to original sources
PubMed1999

Hormonal control of calcium homeostasis.

Calcium homeostasis in the extracellular fluid is tightly controlled and defended physiologically. Hypercalcemia always represents considerable underlying pathology and occurs when the hormonal control of calcium homeostasis is overwhelmed. The major hormones that are responsible for normal calcium homeostasis are parathyroid hormone and 1,25-dihydroxyvitamin D; these hormones control extracellular fluid calcium on a chronic basis. Over- or underproduction of these hormones or the tumor peptide, parathyroid hormone-related peptide, are the major causes of aberrant extracellular fluid calcium concentrations. These hormonal defense mechanisms are reviewed here.

Animals↗
PubMed1992

A novel role for calcite in calcium homeostasis.

Calcium carbonate (CaCO3) minerals are known to be deposited in a wide array of different organisms, ranging from microbes to vertebrates [(1989) On Biomineralization, Oxford University Press, New York]. Calcite, aragonite and vaterite are the major crystalline structural polymorphs of CaCO3 associated with living systems, and participate in a variety of biological functions [(1989) Biomineralization: Chemical and Biochemical Perspectives, VCH Publishers, Weinham, Germany; (1991) Advances in Inorganic Chemistry 36, 137-200]. Here we report on the ability of a soil bacterium to synthesize calcite in a calcium-stressed environment. The elaboration of this exocellular crystalline residue enables the organism to regulate its calcium content. The attainment of calcium homeostasis via the exocellular deposition of bacterial calcite with unique crystal habits is a novel biological phenomenon.

Calcium↗
PubMed1993

The role of calcium homeostasis and calcium currents in ethanol actions on central mammalian neurons.

The ubiquitous role of calcium in ethanol actions measured electrophysiologically in central neurons is discussed. Acute ethanol administration to rat hippocampal neurons in vitro causes a hyperpolarization, increased AHPs, increased EPSPs and IPSPs, decreased modelled electronic interneuronal coupling, decreased high threshold Ca2+ currents, increased Ik, and increased synaptic GABAA currents. Alcohol withdrawal reverses some of these actions. Ca2+ is implicated in all of the above ethanol mediated effects.

Animals↗
PubMed1983

"Calcium antagonists": a class of drugs with a bright future. Part I. Cellular calcium homeostasis and calcium as a coupling messenger.

The aim of this series of minireviews is to present material from multidisciplinary sources to facilitate the understanding of the pharmacology and the ample clinical potential of a class of drugs that were originally designated as "calcium antagonists" and more recently have been referred to as "calcium entry blockers", "calcium slow channel blockers" or "calcium modulators". In this first report our attention will be focussed on the pivotal role of Ca++ as a messenger linking stimuli of extracellular origin to the intracellular environment. Eucaryotic cells have a number of powerful means to control their cytosolic Ca++ concentration. Firstly, in a cell at rest the cellular membrane is relatively impermeable to passive Ca++ movements. This property of the plasmalemma prevents the high free Ca++ concentration (approximately 1 mM) of the extracellular compartment from invading the cytosol (approximately 0.1 microM). However, extracellular Ca++ can reach the cytosol through the Na+/Ca++ exchange mechanism and the plasmalemma possesses special Ca++ channels the conductance of which is controlled by gates that are opened by critical changes in cellular polarization (voltage-operated channels: VOC) or by receptor activation (receptor-operated channel: ROC). The Ca++ entering via VOC or ROC can subsequently trigger the liberation of Ca++ from the sarcoplasmic reticulum or from calcium stores located in the inner side of the plasmalemma. The intracellular message generated by external stimuli is transferred to the response mechanism by several cytosolic proteins that require Ca++ as activator. Finally, the termination of the response is the result of a reduction in the cytosolic Ca++ concentration that is accomplished by the Na+/Ca++ exchange mechanism or by energy-dependent pumps which extrude Ca++ from the cell or store it in subcellular organelles. Therefore, any of the numerous steps of the excitation-response coupling which employ Ca++ as a messenger or as a protein activator can be the site of action of a pharmacological agent. In the follow-up minireview, some methods to determine the basic pharmacological profile of compounds interfering with cellular Ca++-dependent functions will be described.

Action Potentials↗
PubMedDate not supplied

[Calcium homeostasis and calcium-regulating hormones in young children with phenylketonuria].

Calcium and calcium-regulating hormones were investigated in 19 infants with phenylketonuria. Parathyroid hormone, osteocalcin, dehydrocholecalciferol were found elevated while calcitonin reduced in the serum of the infants prior to the diet. Total calcium and phosphorus remained stable in the course of the study. Element diet resulted in reduced serum parathormone levels though surpassing those of healthy subjects. This fact is attributed to primary metabolic disorders responsible for the onset of hyperparathyroidism. The conclusion is made that element diet is unable to change calcium homeostasis and that of calcium-regulating hormones in infants with phenylketonuria.

Calcitonin↗
PubMed1988

Effects of a synthetic peptide of a parathyroid hormone-related protein on calcium homeostasis, renal tubular calcium reabsorption, and bone metabolism in vivo and in vitro in rodents.

A synthetic peptide corresponding to the first 34 amino acids of the parathyroid hormone-related protein (PTH-rP) produced by a human tumor associated with hypercalcemia was examined for skeletal and renal effects on calcium metabolism in vivo and in vitro. These effects were compared with those of human parathyroid hormone (1-34), hPTH (1-34). Equal doses of PTH-rP(1-34) and hPTH(1-34) produced equivalent stimulation of adenylate cyclase in vitro in bone cells and kidney cells and tubules. Subcutaneous injection of PTH-rP(1-34) in mice caused a significant dose-related increase in blood ionized calcium similar to that seen with hPTH(1-34) at equivalent doses. Repeated injections of equal doses of both peptides caused sustained hypercalcemia which was significantly greater in PTH-rP(1-34)-treated mice, although each induced comparable increases in histomorphometric indices of osteoclastic bone resorption. PTH-rP(1-34) and hPTH(1-34) also caused similar increases in bone resorption when incubated with fetal rat long bones in organ culture. Infusion of either peptide into thyroparathyroidectomized rats suppressed urinary calcium excretion and increased urinary excretion of cyclic AMP. PTH-rP appears to have similar effects to those of PTH on the skeleton, the kidney, and overall calcium homeostasis.

Adenylyl Cyclases↗
PubMed1984

Effect of lead intoxication on calcium homeostasis and calcium-mediated cell function: a review.

The interaction between lead and essential metals is a complex, well recognized, but poorly understood phenomenon. Dietary deficiencies or excesses of certain essential metals may alter the absorption, elimination, or dose response of lead. Lead, in turn, may alter the homeostasis and function of essential metals. This review will be limited to the effect of lead on calcium, an essential metal with elaborate systemic and cellular homeostatic mechanisms and innumerable second messenger and coupling-factor functions. Lead may ultimately perturb calcium-regulated or calcium-mediated functions (a) directly by interfering with calcium transport or storage processes, e.g., Ca2+ transport proteins, calcium gates, etc.; (b) indirectly by altering cell functions required for calcium homeostasis, e.g., energy production, plasma membrane permeability, etc.; (c) by substitution of Pb2+ for Ca2+ at functionally important calcium binding sites, e.g., calmodulin. While any individual study may not provide adequate experimental verification of the causal role of perturbations of calcium metabolism and function as the primary toxic lesion of lead intoxication, the collective observations of many studies do strongly support lead-calcium interactions as an important functional lesion in lead intoxicated organelles, cells, tissues, and organ systems.

Animals↗
PubMed1994

The role of pyruvate in neuronal calcium homeostasis. Effects on intracellular calcium pools.

It has long been known that pyruvate is essential for survival of prenatal neurons in culture. To understand the role of exogenous pyruvate in neuronal calcium homeostasis, we have investigated the effects of pyruvate (plus malate) addition to dissociated adult rat hippocampal and cerebral cortex cells and cultured CNS neurons having an unrestricted glucose supply. We found that pyruvate (plus malate) increased the respiration rate while ATP levels were unchanged. At the same time, cytosolic free calcium concentrations, [Ca2+]i, decreased while total 45Ca2+ and 40Ca2+ accumulation increased. The extra Ca2+ accumulated by the cells is attributable to an increase in the size of the intracellular calcium pools. Two such pools were identified on the basis of their sensitivity to specific drugs. The first pool was mobilized by thapsigargin plus tert-butyl hydroquinone and caffeine while the second pool was discharged by the mitochondrial uncoupler carbonyl cyanide p-trifluoromethoxphenylhydrazone (FCCP) (plus oligomycin). The two pools represented about 15-20% and 15-30%, respectively, of the rapidly exchangeable 45Ca2+ pools in cerebral cortex cells. In cultured hippocampal neurons, the collapse of the mitochondrial membrane potential (as induced by uncouplers (FCCP) or respiratory chain inhibitors (antimycin) caused a large increase in [Ca2+]i which varied in size and shape among cells and was reduced by external Ca2+ chelation. The latter condition also resulted in a partial discharge of FCCP-releasable 45Ca2+. The effects of FCCP did not result simply from ATP depletion since incubation in glucose-free medium and sequential additions of 2 mM deoxyglucose and 10 microM oligomycin, conditions that led to a dramatic reduction in cellular ATP levels, did not abolish the FCCP-induced [Ca2+]i rise. Taken together, the results indicate that mitochondria harbor a significant proportion of cellular Ca2+. The sensitivity of the mitochondrial pool size to pyruvate (plus malate) questions previous hypotheses concerning a kinetic limitation for Ca2+ accumulation in mitochondria in resting neurons.

Acetylcholine↗
PubMed2000

Use of recombinant aequorin to study calcium homeostasis and monitor calcium transients in response to heat and cold shock in cyanobacteria.

We investigated the possibility of Ca(2+) signaling in cyanobacteria (blue-green algae) by measuring intracellular free Ca(2+) levels ([Ca(2+)](i)) in a recombinant strain of the nitrogen fixing cyanobacterium Anabaena strain sp. PCC7120, which constitutively expresses the Ca(2+)-binding photoprotein apoaequorin. The homeostasis of intracellular Ca(2+) in response to increasing external Ca(2+) has been studied in this strain. The resting level of free Ca(2+) in Anabaena was found to be between 100 and 200 nM. Additions of increasing concentrations of external Ca(2+) gave a transient burst of [Ca(2+)](i) followed by a very quick decline, reaching a plateau within seconds that brought the level of [Ca(2+)](i) back to the resting value. These results indicate that Anabaena strain sp. PCC7120 is able to regulate its internal Ca(2+) levels. We also monitored Ca(2+) transients in our recombinant strain in response to heat and cold shock. The cell's response to both stresses was dependent on the way they were induced. The use of inhibitors suggests that heat shock mobilizes cytosolic Ca(2+) from both intracellular and extracellular sources, while the Ca(2+) source for cold shock signaling is mostly extracellular.

Aequorin↗
PubMed2005

Lactational transfer of cadmium from Meriones shawi shawi mothers to their pups and its effects on calcium homeostasis and bone calcium in pups.

Cadmium (Cd) was given to Meriones shawi shawi dams in the diet (1 g CdCl2/1.5 kg of diet) from day 1 to day 21 of lactation. Pups were killed at 5, 10, 14 and 21 days of lactation. Thereafter, liver, kidney, femur and stomach content were removed and plasma was collected to element analyses. Cd in stomach content, kidney, liver and femur and calcium (Ca) in stomach content, femur and plasma were determined in pups by atomic absorption spectrophotometer. The results indicate that Cd was transferred to the suckling and it was detected in the liver, the kidney and the femur from the 5th, the 10th and the 14th days of age, respectively. Stomach content of Ca was increased significantly from the 10th day to the end of lactation, whereas Ca levels increase in plasma and femur only at day 10 of lactation.

Animals↗
PubMed2000

Influence of the in vivo calcium status on cellular calcium homeostasis and the level of the calcium-binding protein calreticulin in rat hepatocytes.

Little attention has been given to the consequences of the in vivo calcium status on intracellular calcium homeostasis despite several pathological states induced by perturbations of the in vivo calcium balance. The aim of these studies was to probe the influence of an in vivo calcium deficiency on the resting cytoplasmic Ca2+ concentration and the inositol-1,4,5-trisphosphate-sensitive Ca2+ pools. Studies were conducted in hepatocytes (a cell type well characterized for its cellular Ca2+ response) isolated from normal and calcium-deficient rats secondary to vitamin D depletion. Both resting cytoplasmic Ca2+ concentration and Ca2+ mobilization from inositol-1,4,5-trisphosphate-sensitive cellular pools were significantly lowered by calcium depletion. In addition, Ca deficiency was shown to significantly reduce calreticulin messenger RNA and protein levels but calcium entry through store-operated calcium channels remained unaffected, indicating that the Ca2+ entry mechanisms are still fully operational in calcium deficiency. The effects of calcium deficiency on cellular calcium homeostasis were reversible by repletion with oral calcium feeding alone or by the administration of the calcium-regulating hormone 1,25-dihydroxyvitamin D3, further strengthening the tight link between extra- and intracellular calcium. These data, therefore, challenge the currently prevailing hypothesis that extracellular Ca2+ has no significant impact on cellular Ca2+ by demonstrating that despite the large Ca2+ gradient between extra- and intracellular Ca2+ concentrations, calcium deficiency in vivo significantly alters the hormone-sensitive cellular calcium homeostasis.

Animals↗
PubMed1984

Calcium homeostasis in morbid obesity.

Calcium homeostasis in morbidly obese subjects has attracted little attention. Prompted by reports of elevated serum levels of parathyroid hormone in such patients, calcium homeostasis was investigated in 36 patients with morbid obesity and in 44 normal weight controls. Concerning serum immunoreactive parathyroid hormone (C-terminal), serum ionized calcium (Ca++) and serum albumin corrected magnesium no significant differences between the groups were detected. When albumin corrected, serum total calcium turned out to be significantly elevated (p less than 0.0001) in the obese subjects. Also, serum alkaline phosphatase activity was significantly raised in the obese state. The results demonstrate that calcium homeostasis, as expressed by the metabolically active serum Ca++, is normal in morbid obesity. But the results also point towards an abnormal calcium binding due to either an increased calcium binding to albumin or to calcium complexing small anions.

Adult↗
PubMed2001

Diabetes-induced changes in calcium homeostasis and the effects of calcium channel blockers in rat and mice nociceptive neurons.

AIMS/HYPOTHESIS: Distal neuropathy is the most common complication of diabetes mellitus, making it important to reveal the cellular mechanisms leading to its development, one of which might be the alteration in intracellular calcium homeostasis in primary and secondary nociceptive neurons. We aimed to investigate these possible changes. METHODS: Control and streptozotocin-treated diabetic rats and mice were used. Changes in intracellular free calcium concentrations ([Ca(2+)]i) were measured fluorometrically in primary nociceptive neurons from dorsal root ganglia and in secondary nociceptive neurons from substantia gelatinosa of spinal dorsal horn slices. RESULTS: Measurements of [Ca(2+)]i increases induced in dorsal root ganglion and dorsal horn neurons by membrane depolarization did not show any substantial difference in their peak amplitudes in control and diabetic animals. However, a definite prolongation of the decay phase of the transients was observed under diabetic conditions. Caffeine application to dorsal root ganglion and dorsal horn neurons induced a transient elevation of [Ca(2+)]i which was less prominent in cells from diabetic animals. Short-term application of a calcium channel blocker nifedipine showed a substantial amplification of its action in diabetic neurons. However, chronic administration of nimodipine induced a clear increase in the peak values of transients in dorsal root ganglion neurons of diabetic animals compared with those of untreated animals. CONCLUSION/INTERPRETATION: The described changes of calcium signalling in nociceptive neurons could be the reason for the development of distal polyneuropathy and its symptoms in the early stages of diabetes mellitus.

Animals↗