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PubMed1992

Steady-state and dynamic properties of cardiac sodium-calcium exchange. Secondary modulation by cytoplasmic calcium and ATP.

Dynamic responses of cardiac sodium-calcium exchange current to changes of cytoplasmic calcium and MgATP were monitored and analyzed in giant membrane patches excised from guinea pig myocytes. Secondary dependencies of exchange current on cytoplasmic calcium are accounted for in terms of two mechanisms: (a) The sodium-dependent inactivation process, termed I1 modulation, is itself strongly modulated by cytoplasmic calcium. Recovery from the I1 inactivated state is accelerated by increasing cytoplasmic calcium, and the calculated rate of entrance into I1 inactivation is slowed. (b) A second modulation process, termed I2 modulation, is not sodium dependent. As with I1 modulation, the entrance into I2 inactivation takes place over seconds in the absence of cytoplasmic calcium. The recovery from I2 inactivation is a calcium-dependent transition and is rapid (< 200 ms) in the presence of micromolar free calcium. I1 and I2 modulation can be treated as linear, independent processes to account for most exchange modulation patterns observed: (a) When cytoplasmic calcium is increased or decreased in the presence of high cytoplasmic sodium, outward exchange current turns on or off, respectively, on a time scale of multiple seconds. (b) When sodium is applied in the absence of cytoplasmic calcium, no outward current is activated. However, the full outward current is activated within solution switch time when cytoplasmic calcium is applied together with sodium. (c) The calcium dependence of peak outward current attained upon application of cytoplasmic sodium is shifted by approximately 1 log unit to lower concentrations from the calcium dependence of steady-state exchange current. (d) The time course of outward current decay upon decreasing cytoplasmic calcium becomes more rapid as calcium is reduced into the submicromolar range. (e) Under nearly all conditions, the time courses of current decay during application of cytoplasmic sodium and/or removal of cytoplasmic calcium are well fit by single exponentials. Both of the modulation processes are evidently affected by MgATP. Similar to the effects of cytoplasmic calcium, MgATP slows the entrance into I1 inactivation and accelerates the recovery from inactivation. MgATP additionally slows the decay of outward exchange current upon removal of cytoplasmic calcium by 2-10-fold, indicative of an effect on I2 inactivation. Finally, the effects of cytoplasmic calcium on sodium-calcium exchange current are reconstructed in simulations of the I1 and I2 modulation processes as independent reactions.

Adenosine Triphosphate↗

PubMed1988

Properties of the residual calcium pools in human red cells exposed to transient calcium loads.

1. Inosine-fed human red cells, pre-loaded with calcium with the use of the ionophore A23187, and reincubated at 37 degrees C after ionophore and external calcium removal, pumped calcium out initially fast and then substantially slower when the residual calcium was still very high (García-Sancho & Lew, 1988 a, b). Particularly surprising was the finding of such residual calcium pools in a subpopulation of cells (L cells, García-Sancho & Lew, 1988b) with normal ATP, high active calcium pumping rates, and K+ channels which remained inactive during the density separation procedure (SCN- treatment; García-Sancho & Lew, 1988a). The purpose of the present experiments was to investigate the properties and possible origins of the residual calcium pools. 2. At each ionophore concentration, the pool size increased with the duration and magnitude of the calcium load. At comparable calcium loads, the pool size was smaller the higher the ionophore concentration used. 3. In cells from the same sample, residual calcium pools were present in cells that became dense after SCN- treatment (H cells) as well as those that remained in the light-cell fraction (L cells). Residual calcium was always higher in H cells than in L cells. 4. Re-exposure of cells to ionophore in Ca2+-free media could rapidly extract over 99% of their residual calcium. Residual calcium is therefore in a rapidly mobilizable form within a membrane-bound compartment. 5. Iodoacetamide-induced ATP depletion of H cells with high residual calcium-stimulated calcium loss. Such stimulation could only occur if ATP depletion inhibited a calcium-retaining process within the cells. 6. L cells with high residual calcium may have failed to dehydrate during SCN- treatment because of irreversible K+ channel inactivation or because K+ permeabilization would no longer generate a dehydrating net cation loss. These possibilities were tested and ruled out since it was found that virtually all cells became dense in low-K+, SCN- media after valinomycin addition or re-exposure to A23187 + calcium. 7. The results suggest that part if not all of the residual calcium is contained within compartments with the properties of endocytic inside-out vesicles capable of ATP-dependent calcium accumulation, such as those found in normal and abnormal human red cells (Lew, Hockaday, Sepúlveda, Somlyo, Somlyo, Ortiz & Bookchin, 1985).

Adenosine Triphosphate↗

PubMed1994

Relationship of calcium transients to calcium currents and charge movements in myotubes expressing skeletal and cardiac dihydropyridine receptors.

In both skeletal and cardiac muscle, the dihydropyridine (DHP) receptor is a critical element in excitation-contraction (e-c) coupling. However, the mechanism for calcium release is completely different in these muscles. In cardiac muscle the DHP receptor functions as a rapidly-activated calcium channel and the influx of calcium through this channel induces calcium release from the sarcoplasmic reticulum (SR). In contrast, in skeletal muscle the DHP receptor functions as a voltage sensor and as a slowly-activating calcium channel; in this case, the voltage sensor controls SR calcium release. It has been previously demonstrated that injection of dysgenic myotubes with cDNA (pCAC6) encoding the skeletal muscle DHP receptor restores the slow calcium current and skeletal type e-c coupling that does not require entry of external calcium (Tanabe, Beam, Powell, and Numa. 1988. Nature. 336:134-139). Furthermore, injection of cDNA (pCARD1) encoding the cardiac DHP receptor produces rapidly activating calcium current and cardiac type e-c coupling that does require calcium entry (Tanabe, Mikami, Numa, and Beam. 1990. Nature. 344:451-453). In this paper, we have studied the voltage dependence of, and the relationship between, charge movement, calcium transients, and calcium current in normal skeletal muscle cells in culture. In addition, we injected pCAC6 or pCARD1 into the nuclei of dysgenic myotubes and studied the relationship between the restored events and compared them with those of the normal cells. Charge movement and calcium currents were recorded with the whole cell patch-clamp technique. Calcium transients were measured with Fluo-3 introduced through the patch pipette. The kinetics and voltage dependence of the charge movement, calcium transients, and calcium current in dysgenic myotubes expressing pCAC6 were qualitatively similar to the ones elicited in normal myotubes: the calcium transient displayed a sigmoidal dependence on voltage and was still present after the addition of 0.5 mM Cd2+ + 0.1 mM La3+. In contrast, the calcium transient in dysgenic myotubes expressing pCARD1 followed the amplitude of the calcium current and thus showed a bell shaped dependence on voltage. In addition, the transient had a slower rate of rise than in pCAC6-injected myotubes and was abolished completely by the addition of Cd2+ + La3+.

Animals↗

PubMed1992

Maitotoxin-induced intracellular calcium rise in PC12 cells: involvement of dihydropyridine-sensitive and omega-conotoxin-sensitive calcium channels and phosphoinositide breakdown.

The biological activities of maitotoxin are strictly dependent on the extracellular calcium concentration and are always associated with an increase of the free cytosolic calcium level. We tested the effects of voltage-sensitive calcium channel blockers (nicardipine and omega-conotoxin) on maitotoxin-induced intracellular calcium increase, membrane depolarization, and inositol phosphate production in PC12 cells. Maitotoxin dose dependently increased the cytosolic calcium level, as measured by the fluorescent probe fura 2. This effect disappeared in a calcium-free medium; it was still observed in the absence of extracellular sodium and was enhanced by the dihydropyridine calcium agonist Bay K 8644. Nicardipine inhibited the effect of maitotoxin on intracellular calcium concentration in a dose-dependent manner. The maitotoxin-induced calcium rise was also reduced by pretreating cells with omega-conotoxin. Pretreatment of cells with maitotoxin did not modify 125I-omega-conotoxin and [3H]PN 200-110 binding to PC12 membranes. Nicardipine and omega-conotoxin inhibition of maitotoxin-evoked calcium increase was reduced by pertussis toxin pretreatment. Maitotoxin caused a substantial membrane depolarization of PC12 cells as assessed by the fluorescent dye bisoxonol. This effect was reduced by pretreating the cells with either nicardipine or omega-conotoxin and was almost completely abolished by the simultaneous pretreatment with both calcium antagonists. Maitotoxin stimulated inositol phosphate production in a dose-dependent manner. This effect was reduced by pretreating the cells with 1 microM nicardipine and was completely abolished in a calcium-free EGTA-containing medium. The findings on maitotoxin-induced cytosolic calcium rise and membrane depolarization suggest that maitotoxin exerts its action primarily through the activation of voltage-sensitive calcium channels, the increase of inositol phosphate production likely being an effect dependent on calcium influx. The ability of nicardipine and omega-conotoxin to inhibit the effect of maitotoxin on both calcium homeostasis and membrane potential suggests that L- and N-type calcium channel activation is responsible for the influx of calcium following exposure to maitotoxin, and not that a depolarization of unknown nature causes the opening of calcium channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed2001

Details of true calcium absorption and calcium excretion into feces in female rats during growth.

The details of calcium flux during growth were examined in female rats. Twenty-eight 53-d-old rats were equally divided into 4 groups. Rats were given a purified diet (0.5% Ca and 0.35% Pi) throughout the experiment. Calcium balance and 45Ca kinetics studies using an open two-compartment model were performed over a 3-d period when rats were 60 (control), 74 , 88 and 116 d old. A simple calcium balance study, using the last group, was carried out at the age of 102 d. Compared with the control group, true intestinal calcium absorption was significantly increased at 74 d, but then decreased in a time-dependent manner up to 116 d. The apparent intestinal calcium absorption began to decrease at 88 d, and decreased further with age. An increase in urinary calcium output was observed at 74 and 88 d in phase with calcium excretion into the intestine, and both variables returned to the control level at 116 d. Calcium into bone was decreased at 74 and 116 d. Calcium from bone similarly changed with Vo+ at 74 d: however the highest value was observed at 88 d. Thereafter, Vo- reached the control level at 116 d. Calcium balance rapidly decreased at 88, 102 and 116 d, but still remained positive. Calcium intake remained steady until 102 d, but was significantly decreased at the end of the experiment. The changes in calcium flux with age can be summarized as follows: 1) bone turnover decreased, calcium excretion into the urine and feces began to increase, and true intestinal calcium absorption increased, 2) apparent intestinal calcium absorption decreased, while calcium from bone and calcium excretion into the urine and feces increased, and 3) calcium intake and calcium into bone decreased.

Age Factors↗

PubMed2006

A role for voltage gated T-type calcium channels in mediating "capacitative" calcium entry?

Calcium entry through plasma membrane calcium channels is one of the most important cell signaling mechanism involved in such diverse functions as secretion, contraction and cell growth by regulating gene expression, proliferation and apoptosis. The identity of plasma membrane calcium channels, the main regulators of calcium entry, involved in cell proliferation has been thus extensively sought. Among these, a calcium entry pathway called capacitative calcium entry (CCE), activated by calcium store depletion, is particularly important in non-excitable cells. Though this capacitative calcium entry is generally supposed to occur through TRP channels there is some evidence that voltage-dependent T-type calcium channels may contribute to calcium entry after store depletion. Here we show that though mibefradil, a T-type calcium channel blocker, is able to reduce capacitative calcium entry induced by either thapsigargin or ATP, this was not mimicked by any other T-type calcium channel inhibitors even in cells overexpressing alpha(1H) T-type calcium channels, leading us to conclude that T-type calcium channels are not responsible for the capacitative calcium entry observed in different cancer cell lines. On the contrary, we show that the action of mibefradil on capacitative calcium entry is due to an action on store-operated calcium channels.

Calcium↗

PubMed1997

Partial depletion of sarcoplasmic reticulum calcium does not prevent calcium sparks in rat ventricular myocytes.

1. The exact nature of calcium sparks in the heart remains highly controversial. We sought to determine whether calcium sparks arise from a single or multiple calcium release channels/ ryanodine receptors in the sarcoplasmic reticulum (SR). If their genesis involves a calcium-coupled recruitment of multiple channels, calcium sparks might be abolished by a modest depletion of SR calcium (because of the decrease in unitary calcium flux and hence a decrease in the gain of local calcium-induced calcium release). If, on the other extreme, calcium sparks are produced despite severe SR depletion, the single-channel origin will be preferred. 2. Spontaneous calcium sparks were studied in rat ventricular myocytes using confocal microscopy and the fluorescent calcium probe fluo-3. A computer algorithm was developed to count and measure objectively calcium sparks in linescan images. 3. Thapsigargin (25-150 nM) depleted caffeine-releasable SR calcium by up to 64%, in a dose- and time-dependent manner, without altering the resting cytosolic calcium level. During SR depletion, calcium sparks were robustly observed, albeit at reduced frequency (> or = 30% of control) and amplitude (> or = 60% of control). 4. Due to the reduced detectability of small sparks against noise background, the observed data would overestimate reduction in spark frequency but underestimate amplitude reduction. After correction for this detection bias, we found that the spark frequency was independent of SR load, whereas the amplitude was proportional to load. 5. We conclude that, although spark amplitude depends on SR filling status, the frequency of spark generation is independent of SR calcium load, and therefore independent of the local calcium release rate. This implies that sparks are single-channel events, or collective events that are well above threshold for local regeneration. Additionally, our results suggest that intraluminal SR calcium, at normal or low loads, does not play a major role in the regulation of on-gating of the ryanodine receptor.

Adamantane↗

PubMed2004

Rapid Communication: relative effect of urinary calcium and oxalate on saturation of calcium oxalate.

BACKGROUND: The study compared the effect of urinary calcium with that of oxalate on urinary saturation [relative saturation ratio (RSR)] of calcium oxalate. METHODS: A retrospective data analysis was conducted on urinary stone risk analysis from 667 patients with predominantly calcium oxalate stones. Urinary RSR of calcium oxalate was individually calculated using Equil 2. A "theoretical" curve of the relationship between urinary RSR of calcium oxalate and concentration of calcium or oxalate was obtained at two stability constants for calcium oxalate complex, while varying calcium or oxalate and using group mean values for urinary constituents. RESULTS: At the stability constant of 7.07 x 10(3), the increase in RSR of calcium oxalate was less marked with calcium than with oxalate. However, at the stability constant of 2.746 x 10(3) from the Equil 2 that is considered the "gold standard," calcium and oxalate were equally effective in increasing RSR of calcium oxalate. The above theoretical curves (relating RSR with calcium or oxalate) were closely approximated by the actual curves constructed with data from individual urine samples. Urinary saturation of calcium oxalate was equally dependent on urinary concentrations of calcium and oxalate (r= 0.75 unadjusted and 0.57 adjusted for variables, and P < 0.0001 for calcium; r= 0.73 unadjusted and 0.60 adjusted, P <0.0001 for oxalate). CONCLUSION: Among calcium oxalate stone-formers, urinary calcium is equally effective as urinary oxalate in increasing RSR of calcium oxalate.

Adult↗

PubMed1972

The effect of previous dietary intake of calcium on calcium absorption in rats.

1. The effects are described of the calcium content of diets with a calcium: phosphate ratio of 1 fed to rats during the preceding 6 weeks on aspects of calcium and phosphate metabolism during the seventh week. The apparent absorption of calcium and phosphate, the urinary excretion of calcium and phosphate, the amounts of calcium and phosphate in the carcass and the fasting serum calcium were studied.2. Apparent absorption of calcium and phosphate decreases the longer an animal is on a high calcium diet and the more calcium there is in that diet. Under the same conditions urinary excretion of calcium is increased while urinary excretion of phosphate remains constant.3. The percentage of calcium and phosphate in the carcass is greater the longer an animal is on a high calcium diet and the more calcium there is in the diet, but dietary changes do not affect the serum calcium.4. Apparent absorption of calcium is not correlated with serum calcium but is significantly correlated with percent carcass calcium.5. A distinction is drawn between the effect of the diet currently being consumed (kinetic effect) and the effect of the diet consumed previously (adaptation).6. Changes in apparent absorption of calcium have a greater effect on calcium retention than on changes in urinary excretion.7. The mechanism bringing about the changes in absorption is discussed and it is concluded that serum calcium is unlikely to be the monitored parameter which detects the need for greater absorption; parathyroid hormone is probably not involved.

Adaptation, Physiological↗

PubMed2005

Drosophila mushroom body Kenyon cells generate spontaneous calcium transients mediated by PLTX-sensitive calcium channels.

Spontaneous calcium oscillations in mushroom bodies of late stage pupal and adult Drosophila brains have been implicated in memory consolidation during olfactory associative learning. This study explores the cellular mechanisms regulating calcium dynamics in Kenyon cells, principal neurons in mushroom bodies. Fura-2 imaging shows that Kenyon cells cultured from late stage Drosophila pupae generate spontaneous calcium transients in a cell autonomous fashion, at a frequency similar to calcium oscillations in vivo (10-20/h). The expression of calcium transients is up regulated during pupal development. Although the ability to generate transients is a property intrinsic to Kenyon cells, transients can be modulated by bath application of nicotine and GABA. Calcium transients are blocked, and baseline calcium levels reduced, by removal of external calcium, addition of cobalt, or addition of Plectreurys toxin (PLTX), an insect-specific calcium channel antagonist. Transients do not require calcium release from intracellular stores. Whole cell recordings reveal that the majority of voltage-gated calcium channels in Kenyon cells are PLTX-sensitive. Together these data show that influx of calcium through PLTX-sensitive voltage-gated calcium channels mediates spontaneous calcium transients and regulates basal calcium levels in cultured Kenyon cells. The data also suggest that these calcium transients represent cellular events underlying calcium oscillations in the intact mushroom bodies. However, spontaneous calcium transients are not unique to Kenyon cells as they are present in approximately 60% of all cultured central brain neurons. This suggests the calcium transients play a more general role in maturation or function of adult brain neurons.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed2005

Comparative effects of vitamin K and vitamin D supplementation on calcium balance in young rats fed normal or low calcium diets.

We examined the effect of vitamin K and vitamin D supplementation on calcium balance in young rats fed a normal or low calcium diet. Eighty female Sprague-Dawley rats, 6 wk of age, were randomized by the stratified weight method into eight groups with 10 rats in each group: 0.5% (normal) or 0.1% (low) calcium diet, 0.5% or 0.1% calcium diet+vitamin K (vitamin K2, menatetrenone, 30 mg/100 g, food intake), 0.5% or 0.1% calcium diet+vitamin D (25 microg/100 g, food intake), and 0.5% or 0.1% calcium diet+vitamin K+vitamin D. The duration of the study was 10 wk. Vitamin K supplementation promoted the reduction in urinary calcium excretion and retarded the abnormal elevation of serum PTH level in rats fed a low calcium diet, and stimulated intestinal calcium absorption in rats fed a normal calcium diet. Vitamin D supplementation stimulated intestinal calcium absorption with prevention of the abnormal elevation of serum PTH levels and prevented hypocalcemia in rats fed a low calcium diet, and stimulated intestinal calcium absorption in rats fed a normal calcium diet. The stimulation of intestinal calcium absorption was associated with increased serum 1,25-dihydroxyvitamin D levels. An additive effect of vitamin K and vitamin D on intestinal calcium absorption was found only in rats fed a normal calcium diet. This study shows the differential effects of vitamin K and vitamin D supplementation on calcium balance in young rats fed a normal or low calcium diet.

Animals↗

PubMed1995

Regulation of calcium pump function in back inhibited vesicles by calcium-ATPase ligands.

OBJECTIVE: The aim was to evaluate the effect of changes in substrate-product concentrations of the overall sarcoplasmic reticular Ca(2+)-ATPase reactions on calcium pump function with an emphasis on those factors that modify back inhibition of the pump by intrareticular free calcium. METHODS: Sarcoplasmic reticular vesicles were isolated from the rabbit heart. Calcium uptake by the vesicles was measured with a calcium sensitive minielectrode and was related to ATPase activity, which was measured by the rate of inorganic phosphate (Pi) production or NADH oxidation. Back inhibition was varied by changing [oxalate]. RESULTS: At the high level of back inhibition and low calcium transport efficiency, calcium uptake by sarcoplasmic reticulum was stimulated by pH decrease, hydrophobic compounds, dimethyl sulphoxide, and ATP regeneration. These factors apparently modify either calcium binding to the low affinity binding site of Ca(2+)-ATPase or the effect derived from the binding of calcium to these sites. Under conditions where back inhibition was avoided and calcium transport efficiency was high, the same factors had a depressive effect on calcium uptake. Inorganic phosphate had a dual effect on the rate of calcium uptake supported by low [oxalate]: Pi < 2-3 mM strongly inhibited calcium uptake while further increase in [Pi] reversed this inhibition. At the lower level of back inhibition higher [Pi] was required to inhibit calcium transport. CONCLUSIONS: Changes in [H+], [ADP], and [Pi] can significantly affect calcium pump function, but the effect is dependent on the extent of back inhibition of calcium transport. Changes in the sarcoplasmic reticular Ca(2+)-ATPase environment which mimic those expected to take place at the start of reperfusion (pH increase to 7.0-7.1, high myoplasmic [Ca2+]) may have a depressive effect on the efficiency of calcium transport, provided that intrareticular free calcium is increased. Under those conditions factors able to decrease the inhibitory effect derived from the calcium binding to the low affinity binding sites are expected to improve the efficiency of calcium transport.

Adenosine Triphosphate↗

PubMed1989

Appraisal of the physiological relevance of two hypothesis for the mechanism of calcium release from the mammalian cardiac sarcoplasmic reticulum: calcium-induced release versus charge-coupled release.

Recent studies correlating the calcium current with, respectively, the clamp-imposed voltage and the calcium current in intact isolated mammalian cardiac myocytes are reviewed. The major findings are the following: With the exception of one group, all investigators agree that a calcium transient is never observed in the absence of a calcium current. In addition, there is a good correlation between voltage dependence of the calcium current and that of the calcium transient, although this correlation may vary among the cardiac tissues from different animal species. Repolarization clamp pulses from highly positive potentials produce a 'tail current' which is associated with a 'tail calcium transient'. The calcium transient is inhibited when the calcium current is blocked by calcium deprivation or substitution, or by the addition of calcium current antagonists, despite the fact that sarcoplasmic reticulum still contains calcium that can be released by caffeine (with inhibition of this release by ryanodine). These three findings are strongly in favor of a calcium-induced release of calcium and against the hypothesis of charge-movement-coupled release of calcium from the sarcoplasmic reticulum. The only finding that would be more in favor of the latter hypothesis (although still reconciliable with the former) is that repolarization occurring before the rapid rise of calcium transient is complete curtails the calcium transient. Thus, the possibility that charge movement might somehow regulate calcium-induced release of calcium cannot be excluded.

Animals↗

PubMed2004

Phosphatase inhibition reveals a calcium entry pathway dependent on protein kinase A in thyroid FRTL-5 cells: comparison with store-operated calcium entry.

Calcium entry through store-operated calcium channels is an important entry mechanism. In the present report we have described a novel calcium entry pathway that is independent of depletion of intracellular calcium stores. Treatment of the cells with the phosphatase inhibitor calyculin A (caly A), which blocked thapsigargin-evoked store-operated calcium entry (SOCE), induced a potent concentration-dependent calcium entry. In a calcium-free buffer, acute addition of caly A evoked a very modest increase in cytosolic free calcium ([Ca(2+)](i)). This increase was not from the agonist-mobilizable calcium stores, as the thapsigargin-evoked increase in [Ca(2+)](i) was unaltered in caly A-treated cells. The caly A-evoked calcium entry was not blocked by Gd(3+) or 2-APB, whereas SOCE was. Caly A enhanced the entry of barium, indicating that the increase in intracellular calcium was not the result of a decreased extrusion of calcium from the cytosol. Jasplakinolide and cytochalasin D had only marginal effects on calcium entry. The protein kinase A (PKA) inhibitor H-89 and an inhibitory peptide for PKA abolished the caly A-evoked entry of both calcium and barium. The SOCE was, however, enhanced in cells treated with H-89. In cells grown in the absence of thyrotropin (TSH), the caly A-evoked entry of calcium was smaller compared with cells grown in TSH-containing buffer. Stimulation of cells grown without TSH with forskolin or TSH restored the calyculin A-evoked calcium entry to that seen in cells grown in TSH-containing buffer. SOCE was decreased in these cells. Our results thus suggest that TSH, through the production of cAMP and activation of PKA, regulates a calcium entry pathway in thyroid cells. The pathway is distinctly different from the SOCE. As TSH is the main regulator of thyroid cells, we suggest that the novel calcium entry pathway participates in the regulation of basal calcium levels in thyroid cells.

Actins↗

PubMed1988

Heterogeneous calcium and adenosine triphosphate distribution in calcium-permeabilized human red cells.

1. Calcium permeabilization of inosine-fed human red cells using the divalent cation ionophore A23187 induces pump-leak steady states in which the mean total calcium content of the cells may be held below electrochemical equilibrium for hours. A new method developed to detect and separate cells with different calcium contents revealed a striking heterogeneity of calcium contents in subpopulations of cells in pump-leak steady state (García-Sancho & Lew, 1988a). Most of the mean total cell calcium was found within a fraction of cells rendered dense by the separation procedure (H cells), with relatively little within the remaining light cells (L cells). The experiments in this paper were designed to study the nature and origin of the observed heterogeneity. 2. The fraction of steady-state H cells increased, and the mean ATP content of the cells fell, both linearly, as calcium influx was increased. The H/L divide is therefore the result of a continuous variation in cell properties. When calcium influx was above about 30 mmol/(l cells.h), all cells became dense, calcium distribution was at or near equilibrium, and cell ATP was 0.1-0.2 mmol/l cells. 3. Inosine-fed cells, subjected to ionophore-mediated net calcium influx of 13-15 mmol/(l cells.h), attained a steady state with mean calcium contents far below equilibrium. After ionophore removal and reincubation in calcium-free media, the initial calcium efflux was only a fraction of that required to sustain the previous steady state (less than 25% for H cells, and less than 2% for L cells). The ATP content of L cells was normal whereas that of H cells was irreversibly reduced. These results revealed a paradoxical discrepancy between leak influx and calcium pump efflux in H and L cells which were supposed to have been in steady-state pump-leak balance. 4. The changes in cell calcium and ATP were followed in time after calcium permeabilization to characterize the development of steady-state heterogeneity. Calcium influx triggered a sharp peak in the H cell fraction within 15 s of permeabilization. The mean calcium content of H cells increased towards steady-state values as their fraction decreased; most other cells transferred from H to L density fractions (HL cells) within the first 5 min of permeabilization. 5. In substrate-starved cells calcium influx triggered an immediate fall in cell ATP, steeper in H cells than in L cells. The initial calcium and density transients were unattected.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphate↗

PubMed1996

Increased efficiency of calcium absorption during short periods of inadequate calcium intake in girls.

Adequate calcium intake is essential for skeletal integrity, particularly during the period of peak bone mass acquisition from 9 to 17 y of age. Currently, the calcium intake of many adolescent girls is below the recommended dietary allowance. The purpose of this study was to evaluate the ability of girls to respond to acute periods of inadequate dietary calcium intake. Calcium absorption was evaluated in 11 girls aged 11.6 +/- 2.4 y after 10 d on both a low-calcium (7.05 +/- 2.03 mmol/d) and a high-calcium (35.30 +/- 2.28 mmol/d) diet. Fractional calcium absorption was determined by using oral (46Ca) and intravenous (42Ca) stable isotopes of calcium. During a low calcium intake, fractional calcium absorption was significantly greater (0.582 +/- 0.087 compared with 0.260 +/- 0.068, P < 0.0001) and urinary calcium excretion was significantly lower (1.30 +/- 0.83 compared with 3.08 +/- 1.98 mmol/d, P < 0.004) than values obtained during a high calcium intake. Concentrations of 1,25-dihydroxyvitamin D (combination of cholecalciferol and ergocalciferol) were greater during the low calcium intake, although the difference was not significant (108.7 +/- 30.6 compared with 90.0 +/- 25.1 pmol/L, P < 0.1; n = 9). Excretion of N-telopeptide was significantly greater during the low calcium intake (761 +/- 508 compared with 413 +/- 341 nmol bone collagen equivalent (BCM)/mmol creatinine, P < 0.02; n = 9), indicating that bone resorption was increased. These results suggest that during short periods of inadequate calcium intake, girls are able to significantly increase the efficiency of calcium absorption and decrease urinary calcium losses to conserve calcium required for bone mineral acquisition.

Absorption↗

PubMed1996

Effects of calcium gluconate on the utilization of magnesium and the nephrocalcinosis in rats fed excess dietary phosphorus and calcium.

The effects of calcium gluconate on the utilization of magnesium and nephrocalcinosis in male Wistar rats made magnesium-deficient by adding excess dietary phosphorus (1.195 g of phosphorus/100 g of diet) and calcium (1.04 g of calcium/100 g of diet) were compared with the effects of calcium carbonate. The effects of dietary magnesium concentration on the magnesium status and nephrocalcinosis were also examined. Adding excess dietary phosphorus and calcium decreased the apparent magnesium absorption ratios and the concentrations of magnesium in the serum and femur and increased the deposition of calcium in the kidney, and the low magnesium condition (0.024 g of magnesium/100 g of diet) aggravated the deposition of calcium and the low magnesium status. The apparent magnesium absorption ratios and femur magnesium concentration in the rats fed a calcium gluconate diet (an equimolar mixture of calcium gluconate and calcium carbonate was used as a source of calcium) were significantly higher than in the rats fed a calcium carbonate diet (only calcium carbonate was used as a source of calcium), irrespective of dietary magnesium concentration. Dietary calcium gluconate lessened the accumulation of calcium in the kidney and increased the serum magnesium concentration compared with dietary calcium carbonate, when the rats were fed the normal magnesium diet (0.049 g of magnesium/100 g of diet) but not the low magnesium diet. We speculate that the increased utilization of magnesium by feeding the calcium gluconate diet to a limited extent prevented the low magnesium status and the severity of nephrocalcinosis caused by adding excess dietary phosphorus and calcium.

Absorption↗

PubMed2002

Calcium-induced calcium release participates in cell volume regulation of rabbit TALH cells.

Changes of cell volume and intracellular calcium concentration ([Ca(2+)](i)) in immortalized thick ascending limb of Henle's loop (TALH) cells were monitored using confocal laser scanning microscopy and fura-2 fluorescence, respectively. Reduction of the extracellular osmolarity from 600 to 300 mosmol/l induced cell swelling followed by regulatory volume decrease (RVD). Simultaneously, the [Ca(2+)](i) increased transiently. The calcium rise was not observed in calcium-free solution or in the presence of nifedipine, indicating that the change was, in the first place, due to the activation of a calcium influx. Application of ATP or caffeine in isotonic solutions increased transiently the [Ca(2+)](i) which revealed the existence of stores in TALH cells sensitive to inositol-1,4,5 trisphosphate (IP(3)) and ryanodine. To examine the possibility that the calcium influx might induce calcium release, manganese quenching experiments were performed. In hypotonic calcium-free solutions, the decay of the calcium-insensitive and calcium-sensitive fluorescence occurred simultaneously. In the presence of extracellular calcium however, the calcium-sensitive wavelength revealed initial calcium influx followed by a calcium release from intracellular stores. Thus, the calcium influx was a prerequisite for the calcium release. We conclude that calcium-induced calcium release participates in global calcium signalling during RVD of TALH cells.

Animals↗