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PubMed1987

Calcium channels, the sodium-calcium exchange and intracellular sodium in the predisposition of the heart to the calcium paradox.

A wide variety of cardiac tissues load with Na+ on exposure to Ca-free fluid. This loading is due to a sustained influx of Na+ through the calcium channels and predisposes the tissues to the changes known as the Calcium Paradox on reperfusion with calcium containing fluid. The cells then load with calcium, most probably via activation of the Na/Ca exchange. This calcium loading may be responsible for the subsequent changes in intracellular pH and cellular metabolism.

Action Potentials↗

PubMed1989

[Comparison of calcium oxalate values as indicators of risk for calcium oxalate calcinosis and the degree of urine saturation in patients with calcium urolithiasis and in healthy patients].

Daily excretion of calcium, magnesium, oxalates, and citrates together with daily urine output were determined in 37 patients with calcium urolithiasis and in 25 healthy individuals. Basing on the obtained values, a degree of urine saturation with calcium oxalate with Marshall and Robertson technique and a value of risk factor with Tiselius technique were calculated. It was found that daily diuresis and excretion of calcium with the urine are significantly higher in patients with urolithiasis where as daily excretion of citrates with the urine is significantly lower than in healthy individuals. Risk index proved two-fold higher in the examined patients than in the healthy individuals (p greater than 0.001) while the degree of urine saturation with calcium oxalate did not differ significantly in both groups. The authors, discussing causes of seemingly different changes in both tested parameters, stressed diagnostic value of risk index which includes excretion of crystallization inhibitors (magnesium, citrates) and contrary to the degree of urine saturation is independent of daily urine output.

Adult↗

PubMed2000

Calcium influx through calcium leak channels is responsible for the elevated levels of calcium-dependent proteolysis in dystrophic myotubes.

To estimate calpain proteolysis, we measured the hydrolysis rate of a fluorogenic calpain substrate in individual resting normal and dystrophic mdx mouse myotubes in culture. Hydrolysis rates were high during myoblast and myotube alignment and fusion. After alignment and fusion ceased, hydrolysis rates declined. For normal myotubes, hydrolysis remained low after the development of contractile activity. In contrast, after the development of contractile activity, dystrophic mdx myotubes had abnormally high levels of hydrolysis that were dependent on external calcium and that could be abolished by calpeptin, an inhibitor of calpain. We eliminated the direct effects of contraction during measurements of hydrolysis by the addition of tetrodotoxin. Substrate hydrolysis by lysosomes or proteosomes was controlled for using NH(4)Cl and clasto-lactacystin beta-lactone, respectively. Increased activity of the calcium-activated protease in mature mdx myotubes was linked to the abnormal activity of calcium-specific leak channels because an antagonist of these channels reduced the higher levels of hydrolysis in dystrophic myotubes to nearly normal levels. The abnormal activity of these channels is linked to an increased frequency of transient sarcolemmal disruptions in the more fragile mdx myotubes (, ). Treatment of mdx myotubes with a pro-drug of methylprednisolone also reduced calpain substrate hydrolysis to nearly normal levels. However, this inhibition only required 2.5 h of pretreatment, which was not long enough to act by the known effects of prednisolone on calcium homeostasis.

Ammonia↗

PubMed1991

8-Diethylamino-octyl-3,4,5-trimethoxybenzoate, a calcium store blocker, increases calcium influx, inhibits alpha-1 adrenergic receptor calcium mobilization, and alters iodide transport in FRTL-5 rat thyroid cells.

8-Diethylamino-octyl-3,4,5-trimethoxybenzoate (TMB-8) is known to inhibit mobilization of calcium from intracellular stores but, more recently, other cellular effects have been described. In the present study, the effects of TMB-8 on cytosolic free calcium [Ca2+]i levels in FRTL-5 rat thyroid cells were determined using the fluorescent dye, Indo-1. TMB-8 increased [Ca2+]i in a dose-dependent manner, with a maximum rise from 120 +/- 7 nM to 229 +/- 16 nM (90 +/- 5% increase) at 5 x 10(-4) M. This effect was considerably reduced in Ca2+ free buffer, demonstrating a dependency upon extracellular calcium influx but not upon membrane potential and which did not involve the Na+/Ca2+ exchanger. In Ca2+ free buffer TMB-8, at a dose which did not affect [Ca2+]i, completely prevented norepinephrine (10(-5) M) from mobilizing intracellular Ca2+. To determine whether TMB-8 affected differentiated functions, iodide uptake and efflux studies were performed with 125I. TMB-8 (10(-4) M) inhibited iodide uptake by approximately 40% without affecting efflux. At 10(-3) M TMB-8, efflux was also enhanced. These studies demonstrate that TMB-8 has at least two effects on [Ca2+]i, promoting calcium influx and preventing alpha-1 adrenergic mobilization from intracellular stores. TMB-8 also has multiple effects on 125I transport, both inhibiting influx and increasing efflux. The results emphasize the importance of characterizing the behavior of this compound in any cell system before using it as a biological probe.

Animals↗

PubMedDate not supplied

Inhibitors of calmodulin-dependent phosphorylation simultaneously inhibit calcium uptake and calcium-dependent ATPase activity in skeletal muscle sarcoplasmic reticulum and transiently induce calcium release.

Under adequate experimental conditions calmodulin antagonists like compound 48/80 do not dissociate calcium uptake from the calcium-dependent ATP hydrolysis of skeletal muscle sarcoplasmic reticulum membranes but simultaneously inhibit both processes. Apart from the agent's pump inhibiting effect, they interact with the caffeine sensitive calcium channel in the sarcoplasmic reticulum causing a rapid transient calcium release.

Caffeine↗

PubMed2000

The effect of calcium-sensing receptor gene polymorphisms on serum calcium levels: a familial hypocalciuric hypercalcemia family without mutation in the calcium-sensing receptor gene.

Familial hypocalciuric hypercalcemia (FHH) is a benign syndrome with elevated levels of serum calcium, relative hypocalciuria, and non-suppressed serum parathyroid hormone (PTH) levels. FHH usually occurs by a heterozygous mutation of the calcium sensing receptor (Casr), but some FHH patients show no mutations of the Casr. We encountered a unique FHH family in which the proband and her mother had many calcium deposits on their skin. The proband was medicated with Levothyroxine for hypothyroidism due to an iodine transport defect (ITD). We searched for mutation of the Casr, but found none. The only change distinguishing the proband and her mother from her father was at codon 990, reported to be a polymorphic site. We investigated the frequency of polymorphism at codon 990, but a significant relationship between the three genotypes and the serum calcium concentration was excluded. At the other polymorphic sites at codon 536, 926, 986, and 1011, polymorphisms were rare in Japanese, and we could not confirm a significant relationship. In conclusion, mutation in the Casr gene alone does not explain all cases of FHH. The other mechanisms should be identified.

Base Sequence↗

PubMed1992

Effect of vitamin D3 administration on the serum calcium and inorganic phosphate levels of the freshwater catfish, Heteropneustes fossilis, maintained in artificial fresh water, calcium-rich fresh water, and calcium-deficient fresh water.

Freshwater catfish, Heteropneustes fossilis, were injected daily intraperitoneally either with vehicle (0.05 ml of 95% ethanol/100 g body wt) or vitamin D3 (50 I.U./100 g body wt) and maintained in artificial fresh water, calcium-rich fresh water, or calcium-deficient fresh water for 10 days. The specimens were sacrificed on Days 1, 3, 5, and 10 after initiation of the experiment. The blood samples were collected on these intervals and serum calcium and inorganic phosphate levels were analyzed. Vitamin D3 induced hypercalcemia and hyperphosphatemia in the freshwater catfish, H. fossilis. These effects of vitamin D3 are not dependent upon the calcium concentration of the different ambient media used in this study.

Animals↗

PubMed1987

Isolation from human calcium oxalate renal stones of nephrocalcin, a glycoprotein inhibitor of calcium oxalate crystal growth. Evidence that nephrocalcin from patients with calcium oxalate nephrolithiasis is deficient in gamma-carboxyglutamic acid.

We have determined that the organic matrix of calcium oxalate kidney stones contains a glycoprotein inhibitor of calcium oxalate crystal growth (nephrocalcin) that resembles nephrocalcin present in the urine of patients with calcium oxalate stones and differs from nephrocalcin from the urine of normal people. Pulverized calcium oxalate renal stones were extracted with 0.05 M EDTA, pH 8.0; nephrocalcin eluted in five peaks using DEAE-cellulose column chromatography, and each peak was further resolved by Sephacryl S-200 column chromatography. Four of the five DEAE peaks corresponded to those usually found in nephrocalcin from urine; the fifth eluted at a lower ionic strength than any found in urine. Amino acid compositions and surface properties of nephrocalcins isolated from kidney stones closely resembled those of nephrocalcins isolated from urine of stone-forming patients: they differed from normal in lacking gamma-carboxyglutamic acid residues, and in forming air-water interfacial films that were less stable than those formed by nephrocalcin from normal urine.

1-Carboxyglutamic Acid↗

PubMed1992

Urine calcium and serum ionized calcium, total calcium and parathyroid hormone concentrations in the diagnosis of primary hyperparathyroidism and familial benign hypercalcaemia.

A relationship between serum concentrations of ionized calcium and parathyroid hormone (PTH) in persons without parathyroid overactivity was defined by performing an oral calcium load test. As a result, a serum PTH concentration greater than 2.6 pmol/L in a hypercalcaemic patient was regarded as suggestive of hyperparathyroidism. Fasting serum PTH concentrations in 58 patients with surgically and histologically proven primary hyperparathyroidism (PHPT) were all above 2.7 pmol/L (range 3.2-84.5). Thirteen of 20 patients with familial benign hypercalcaemia (FBH) had fasting serum PTH concentrations greater than 2.6 pmol/L (range 1.6-6.1). There was a significant correlation between serum PTH and age in the FBH patients only. Fasting urine calcium excretion (CaE) ranged from 14 to 222 mumol/L of glomerular filtrate in PHPT and 3-34 mumol/L of glomerular filtrate in FBH. The best biochemical discriminant between patients with PHPT and FBH was a plot of fasting serum PTH against CaE. A plot of post-calcium load PTH against post-load CaE showed no further significant advantage in discriminating between the two conditions.

Adolescent↗

PubMed1991

Dissociation of calcium from the phosphorylated calcium-transporting adenosine triphosphatase of sarcoplasmic reticulum: kinetic equivalence of the calcium ions bound to the phosphorylated enzyme.

The internalization of 45Ca by the calcium-transporting ATPase into sarcoplasmic reticulum vesicles from rabbit muscle was measured during a single turnover of the enzyme by using a quench of 7 mM ADP and EGTA (25 degrees C, 5 mM MgCl2, 100 mM KCl, 40 mM MOPS.Tris, pH 7.0). Intact vesicles containing either 10-20 microM or 20 mM Ca2+ were preincubated with 45Ca for approximately 20 s and then mixed with 0.20-0.25 mM ATP and excess EGTA to give 70% phosphorylation of Etot with the rate constant k = 300 s-1. The two 45Ca ions bound to the phosphoenzyme (EP) become insensitive to the quench with ADP as they are internalized in a first-order reaction with a rate constant of k = approximately 30 s-1. The first and second Ca2+ ions that bind to the free enzyme were selectively labeled by mixing the enzyme and 45Ca with excess 40Ca, or by mixing the enzyme and 40Ca with 45Ca, for 50 ms prior to the addition of ATP and EGTA. The internalization of each ion into loaded or empty vesicles follows first-order kinetics with k = approximately 30 s-1; there is no indication of biphasic kinetics or an induction period for the internalization of either Ca2+ ion. The presence of 20 mM Ca2+ inside the vesicles has no effect on the kinetics or the extent of internalization of either or both of the individual ions. The Ca2+ ions bound to the phosphoenzyme are kinetically equivalent. A first-order reaction for the internalization of the individual Ca2+ ions is consistent with a rate-limiting conformational change of the phosphoenzyme with kc = 30 s-1, followed by rapid dissociation of the Ca2+ ions from separate independent binding sites on E approximately P.Ca2; lumenal calcium does not inhibit the dissociation of calcium from these sites. Alternatively, the Ca2+ ions may dissociate sequentially from E approximately P.Ca2 following a rate-limiting conformational change. However, the order of dissociation of the individual ions can not be distinguished. An ordered-sequential mechanism for dissociation requires that the ions dissociate much faster (k greater than or equal to 10(5) s-1) than the forward and reverse reactions for the conformational change (k-c = approximately 3000 s-1). Finally, the Ca2+ ions may exchange their positions rapidly on the phosphoenzyme (kmix greater than or equal to 10(5) s-1) before dissociating. A Hill slope of nH = 1.0-1.2, with K0.5 = 0.8-0.9 mM, for the inhibition of turnover by binding of Ca2+ to the low-affinity transport sites of the phosphoenzyme was obtained from rate measurements at six different concentrations of Mg2+.

Adenosine Diphosphate↗

PubMed1999

Physical properties and self-setting mechanism of calcium phosphate cements from calcium bis-dihydrogenophosphate monohydrate and calcium oxide.

An apatitic calcium phosphate cement was developed from calcium bis-dihydro-genophosphate monohydrate (or monocalcium phosphate monohydrate, MCPM) and calcium oxide (CaO). The powder had a Ca/P molar ratio of 1.67, and the liquid was either pure water or 0.25 M-1 M sodium phosphate buffer, pH 7.4. The influence of the powder-to-liquid (P/L) ratio on the setting time and the mechanical strength were studied. The best results were obtained for the 1 M phosphate buffer with a P/L ratio of 1.53; the setting time was 7 min and the compressive strength was 25 MPa after 24 h and 33 MPa after 11 d. The mechanism and kinetics of the setting reaction were investigated by X-ray diffraction, differential scanning calorimetry, 31P magic angle spinning-nuclear magnetic resonance and infrared spectrometry. The setting reaction was found to be biphasic: in the first step, during the mixing time, MCPM reacted with CaO immediately to give calcium hydrogenophosphate dihydrate (or dicalcium phosphate dihydrate, DCPD) which, in the second step, reacted more slowly with the remaining CaO to give hydroxyapatite. The conversion of the starting materials to hydroxyapatite was complete within 24 h when the liquid was water, but was slower and incomplete with the phosphate buffers. Of the starting materials, 30% remained after 3 d.

Journal Article↗

PubMed1987

The calcium-sensitive dye arsenazo III inhibits calcium transport and ATP hydrolysis by the sarcoplasmic reticulum calcium pump.

The calcium-sensitive dye, arsenazo III, was found to interact with sarcoplasmic reticulum vesicles and to inhibit markedly the rate of calcium transport and ATP hydrolysis by these vesicles, thus perturbing the transport process it was meant to monitor. Caution should therefore be exercised when using this dye to monitor calcium movements.

Adenosine Triphosphate↗

PubMed1994

A phospholipase A2 inhibitor (Ro 31-4493) prevents protein loss associated with the calcium paradox in isolated guinea pig hearts without effect on contracture, calcium overload, or the currents through L-type calcium channels.

OBJECTIVE: Although it is widely accepted that the hypercontraction provoked by the influx of Ca2+ on return to normal Tyrode solution after a period of Ca2+ depletion (the calcium paradox) contributes to the damage to the cell membrane, it remains possible that the Ca2+ overload activates intracellular enzymes that are important in the initial degradation of the cell membrane. This possibility was examined in this work. EXPERIMENTAL DESIGN: The effect of Ro 31-4493, a phospholipase A2 inhibitor, upon protein loss, hypercontracture, and ultrastructural changes in Langendorff perfused guinea pig hearts during the calcium paradox was studied. Because the degree of Ca2+ overload might also be affected, the action of the drug on the resting and action potentials and the whole cell currents through the L-type Ca2+ channels and the changes in [Ca2+]i in isolated guinea pig ventricular myocytes were also studied. RESULTS: Ro 31-4493, at 10-50 microM, inhibited the release of proteins from guinea pig Langendorff perfused hearts during the calcium paradox in a dose dependent way. This protective effect required preincubation with the agent before the Ca2+ depletion. No significant effect upon the contractile behaviour, as recognised from the sustained increase in intraventricular pressure on Ca2+ repletion, was produced. However, structural changes suggest that the extent of hypercontraction, the disruption of cell membrane and the release of mitochondria was less in treated hearts. Ro 31-4493 produced no change in the resting and action potentials or the behaviour of the L-type Ca2+ channels with either Ca2+ or Na+ as the charge carrier, while measurements of [Ca2+]i indicated a similar Ca2+ overload in both treated and untreated hearts. CONCLUSION: The effects of Ro 31-4493 are inconsistent with mechanical consequences of hypercontraction upon activation of a Ca2+ dependent phospholipases may be an important step.

Action Potentials↗

PubMed1997

Elevating intracellular calcium levels in human sperm using an internal calcium ATPase inhibitor, 2,5-di(tert-butyl) hydroquinone (TBQ), initiates capacitation and the acrosome reaction but only in the presence of extracellular calcium.

The aim of this study was to investigate the effect of an internal calcium ATPase inhibitor, TBQ, on human sperm capacitation and the acrosome reaction during incubation in a calcium-depleted media. Sperm were isolated into and incubated for up to 6 hr in media depleted of Ca2+ and two Ca(2+)-containing media controls. At set time intervals, sperm in each media group were treated with 100 microM TBQ for 5 min. Afterwards, sperm were induced to acrosome react using the divalent cation ionophore, A23187, as a measure of sperm fertilizing potential. It was established, using the Chlortetracycline assay, that incubation of sperm in a Ca(2+)-depleted media inhibited or delayed sperm capacitation resulting in fewer spontaneous or A23187-induced acrosome reacted sperm. However, incubation of sperm in a Ca(2+)-depleted media did not appear to inhibit sperm motility. The treatment of sperm with TBQ during their incubation in Ca(2+)-depleted media was found to have very little effect resulting in low numbers of capacitated and acrosome reacted sperm. The results from this study suggest that human sperm have an obligatory requirement for extracellular calcium during capacitation and the acrosome reaction, but may require either very little extracellular Ca2+ to maintain motility or possess internal Ca2+ stores sufficient for their requirements. In addition, TBQ did not increase the number of capacitated and acrosome reacted sperm during incubation in a Ca(2+)-depleted media suggesting that the TBQ-effect of accelerating sperm capacitation is dependent on presence of extracellular Ca2+.

Acrosome↗

PubMed2004

Calcium absorption measurements in normal subjects in determining calcium deposition during prolonged hypokinesia and with and without calcium loading.

Measuring calcium (Ca) absorption, Ca balance and Ca level in serum,feces and urine during HK (hypokinesia) with and without Ca loading, the aim of this study was to disclose if prolonged HK could reduce Ca deposition more with or without Ca load contributing to greater Ca imbalance. Studies were conducted during 30-days pre-HK and 364-days HK. Forty male normal volunteers 23.7+/-6.0 years of age were chosen as subjects. They were divided into four groups: unloaded active control subjects (UACS), unloaded hypokinetic subjects (UHKS), loaded active control subjects (LACS), loaded hypokinetic subjects (LHKS). All hypokinetic subjects were walking average distances of 0.5+/-0.2 km day(-1), and active control subjects were running average distances of 6.6+/-1.2 km day(-1). LACS and LHKS were loaded with 1.3 mmol calcium lactate/kg body wt. Before Ca load, fecal Ca loss, urinary Ca and phosphate (P) losses, Ca imbalance, serum ionized calcium (CaI), P and total Ca (Ca(t)) levels increased significantly. (P < 0.05) with time, and serum intact parathyroid hormone (iPTH), 1.25 dihydroxyvitamin D (1.25(OH)2D3) levels and Ca absorption, decreased significantly (P < 0.05) with time in LHKS and UHKS compared with their pre-HK values and their respective active controls (LACS and UACS). After Ca load, however, Ca absorption, serum iPTH and 1.25 (OH)2D3 levels decreased significantly (P < 0.05) more with time, while fecal Ca loss, urinary Ca and P excretion and Ca imbalance increased significantly (P < 0.05) more with time in LHKS than UHKS. Conversely, before and after Ca load, fecal Ca excretion, urinary P and Ca loss, serum CaI, P, Ca, iPTH and 1.25 (OH)2D3 levels, Ca absorption and Ca balance did not change in LACS and UACS compared with their pre-HK values. The greater Ca losses with than without Ca load have shown that the more Ca is consumed the more Ca is eliminated during HK and Ca imbalance. The significant increase of Ca loss with Ca imbalance demonstrated reduced Ca deposition. Dissociation between Ca loss and Ca imbalance demonstrated reduced Ca deposition as the mechanism of Ca imbalance development during HK.

Absorption↗

PubMed1991

Thimerosal causes calcium oscillations and sensitizes calcium-induced calcium release in unfertilized hamster eggs.

Calcium-induced-calcium-release (CICR) was assayed in unfertilized golden hamster eggs by injecting Ca2+ and monitoring Ca2(+)-dependent hyperpolarizing responses (HRs) and Ca2(+)-sensitive fluo-3 fluorescence. Incubating eggs in the sulfhydryl reagent thimerosal caused [Ca2+]i oscillations as monitored by Ca2(+)-dependent HRs and decreased approximately 10-fold the Ca2+ injection current required to generate an HR and cause a large intracellular Ca2+ increase. Thimerosal also enhanced the sensitivity of eggs to Ca2+ injection in a calcium-free medium. The effects of thimerosal on CICR were prevented by dithiothreitol and were not mimicked by injecting inositol 1,4,5-trisphosphate. The data suggest that thimerosal may be an alternative agent for studying CICR in caffeine-insensitive cells.

Animals↗

PubMed1994

Localization of calcium entry through calcium channels in olfactory receptor neurones using a laser scanning microscope and the calcium indicator dyes Fluo-3 and Fura-Red.

The intracellular calcium concentration [Ca2+]i in olfactory receptor neurones of Xenopus laevis was imaged with high spatial and temporal resolution. A new method using a mixture of the calcium indicator dyes Fluo-3 and Fura-Red was employed. The fluorescence patterns in two wavelength bands were measured on the emission side of a confocal laser scanning microscope, and the ratio R of the fluorescence intensities was taken as an estimate of [Ca2+]i. When the neurones were depolarized by elevating the extracellular potassium concentration [K+]o they showed one of three types of responses: a fast increase in [Ca2+]i, a slow increase in [Ca2+]i, or no change in [Ca2+]i. The fast increase in [Ca2+]i took place in the soma compartment. For at least 4 s after the onset of depolarization the calcium distribution in the dendrite remained essentially unchanged. To study the fast increase with high time resolution, line scan images were taken. The neurones were depolarized for brief periods applying a solution containing high [K+] onto the soma from an application pipette. The fast increase in [Ca2+]i began with a delay of about 200 ms and went from the resting concentration to about 110 nM above resting concentration. Following the depolarization, recovery from elevated [Ca2+]i to resting levels had a time constant of about 15 s. The slow response seemed to depend on the removal of [Na+] from the bath rather than on the elevated [K+] in the bath. The response was also observed with Cd2+, Ni2+, and Co2+ (1.5 mM each) in the bath.(ABSTRACT TRUNCATED AT 250 WORDS)

Aniline Compounds↗

PubMed1983

Urinary cAMP and calcium excretion in the fasting state and their response to oral calcium loading in patients with calcium urolithiasis.

Fifty-two patients with idiopathic calcareous urolithiasis (ICU) were studied with an oral calcium loading test. Twenty-one subjects were normo-calciuric with no other detectable abnormalities (NDA). Of 31 patients with hypercalciuria, 16 had elevated fasting urinary calcium excretion (UCaE) (HFC), and 15 had normal UCaE (NFC). The fasting UCaE was significantly higher and the theoretical renal threshold for phosphate (TmPO4) was significantly lower in ICU patients as compared to 19 control individuals. The mean post oral calcium loading (Post Ca) UCaE rose significantly in hypercalciuric patients compared with control subjects; however, only 18/31 (58 per cent) had values above the normal range. There was no correlation between the fasting UCaE and either the immunoreactive parathyroid hormone (iPTH) or nephrogenous cAMP (ncAMP) in ICU patients. The fasting ncAMP was normal in all subjects with ICU and 7 of 52 subjects had elevated fasting iPTH values. When ranked according to the fasting UCaE value, ICU patients formed a continuum in which the NDA and HFC groups represented the extremes. It is concluded that the responses to oral Ca loading serve no useful role in the identification of an individual ICU patient either in terms of the pathogenetic subgroup or in the differentiation from normal controls.

Administration, Oral↗