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PubMed1984

Calcium exchange and ionized cytoplasmic calcium in resting and activated human monocytes.

We have performed a comprehensive study of calcium tracer flux, distribution, content, and ionized cytoplasmic calcium during monocyte activation. A model of monocyte calcium was developed from 45Ca uptake and exodus curves which indicated that cell calcium was partitioned between three compartments. The magnitude of the time constants for each pool lead us to propose cellular locations for these three compartments: a surface plasma membrane pool, a cytoplasmic pool, and an organelle pool. 45Ca uptake and exodus experiments were analyzed using a nonlinear least squares fit of compartmental exchange rates and sizes. The production of superoxide was used as a reflection of the state of activation of the monocytes treated with Concanavalin A (Con A). We found that Con A-treated monocytes have an increase in the calcium exchange rate with the cytoplasmic pool from 0.04 to 0.07/min (P less than 0.05), and an increase in the size of the cytoplasmic pool from 0.08 to 0.13 pmol/cell (P less than 0.05). There were no significant changes in the exchange rates or sizes associated with either of the other two compartments. The cytoplasmic ionized calcium was measured with the fluorescent probe, Quin 2, which indicated a resting level of 83 nM free calcium in unadhered monocytes. Con A stimulation caused a doubling of the cytoplasmic free calcium to 163 nM within 45 s. This increment in cytoplasmic free calcium preceded the onset of superoxide following Con A treatment. These studies indicate that Con A binding to the plasma membrane increases the monocyte plasma membrane permeability to calcium. External calcium enters the cell at an increased rate and contributes to both internally bound and free calcium. The magnitude of the increase in free calcium is proportional to the concentration of Con A and stimulates calcium extrusion via the calcium transport ATPase. Moreover, there is an increased concentration of ionized cytoplasmic calcium which has the potential to interact with other cellular regulators that modulate cell activation and superoxide production.

Biological Transport, Active↗

PubMed1998

Calcium-regulated renal calcium handling in healthy men: relationship to sodium handling.

Several studies have shown an increase in urinary calcium excretion in response to a calcium load. However, because of the inverse changes in PTH levels with a calcium load, the effect of changes in serum calcium per se on its own excretion is unclear in humans. In this study we used a PTH clamp protocol to further characterize calcium-regulated renal calcium and magnesium handling and the relationship of the former to sodium excretion. Eight normal male subjects were evaluated using a calcium clearance protocol with graded calcium infusions under a PTH clamp while in balance during a high and then during a low sodium diet. The curves describing calcium and magnesium excretion as a function of serum ionized calcium on the high sodium diet were best fitted by sigmoidal functions, with midpoints (the levels of calcium resulting in half-maximal increases in urinary cation excretion) of 1.51 and 1.49 mmol/L, respectively. The curve describing urinary sodium as a function of serum calcium was also sigmoidal on the high sodium diet, with a midpoint of 1.55 mmol/L. Our data taken in conjunction with those of previous studies evaluating sodium and calcium excretion in diseases characterized by inactivating or activating mutations in the calcium receptor, are consistent with the hypothesis that PTH-independent, calcium-dependent changes in renal calcium, magnesium, and sodium handling may be mediated at least in part by this receptor, which is known to be located in the loop of Henle.

Adult↗

PubMed1984

Effects of various levels of dietary calcium during pregnancy on maternal calcium utilization and fetal growth in rats.

The effects of calcium-free and normal (0.6%) and high (1.0%) calcium diets on the transfer of calcium from pregnant mothers to fetuses were investigated by balance experiments. Pregnant rats receiving calcium-free, normal and high calcium diets ate totals of 353, 324 and 280 g of the diet, respectively, during pregnancy, and the food consumption of the latter two groups decreased near term. The group on calcium-free diet was able to maintain pregnancy and produce normal fetuses by using calcium resorbed from the dam's bones. The calcium retentions due to pregnancy in rats on normal and high calcium diets were 116 and 128 mg, respectively, during the first 15 days, and -9 and -109 mg, respectively, during the last 6 days of pregnancy. Fetuses contained about 130 mg of calcium at term and most of this calcium was supplied from the dam's bones, in which extra calcium were retained during early-mid pregnancy. Unexpectedly, the true rate of calcium absorption was appreciably lower during late pregnancy than during early-mid pregnancy in both dietary groups. Thus, extra calcium retention during early-mid pregnancy seemed to be physiological adaptation to a decrease in either food consumption or calcium absorption during late pregnancy. Phosphorus absorption and its balance were examined in relation with the dietary calcium levels.

Animals↗

PubMed1990

Effect of a calcium-enriched diet on the colonic epithelial hyperproliferation induced by N-methyl-N'-nitro-N-nitrosoguanidine in rats on a low calcium and fat diet.

We examined whether hyperproliferation of colonic crypt epithelium during cancer induction by N-methyl-N-nitro-N-nitrosoguanidine (MNNG), in rats on a low fat and calcium diet could be reduced by added calcium p.o. From the age of 4 weeks, 104 male Sprague-Dawley rats received a low fat (3.5%), low calcium (0.05% calcium ion), and low vitamin D (0.4 IU/g) diet. Sixty-four also had calcium salts, derived from either calcium lactate or solubilized calcium carbonate, added to their drinking water; therefore their total calcium intake was about 1% of daily diet. At age 12 weeks the rats were divided into 4 treatment groups: 8 rats, not receiving added calcium, had rectal saline instillations weekly (saline control group) and were sacrificed after a further 28 weeks; 3 groups of 32 rats each received intrarectal MNNG (1.5 mg) weekly. One group, not receiving added calcium, was the MNNG control group; while the second group also received added calcium lactate, and the third group received calcium carbonate. Groups of 24 were sacrificed periodically until 28 weeks of treatment. Rats were sacrificed and epithelial proliferation was estimated, 1 week after the last intrarectal instillation, by in vivo labeling with tritiated thymidine and measuring the ratio of labeled to total colonic crypt epithelial cells. The mean labeling index of the MNNG treated and added calcium groups were significantly higher (8.7-9.5%) than that of the saline controls (2.8%) only at week 28; however, it was then still significantly less than that of the MNNG controls not having added calcium (17.9%). Hyperproliferation, during induction of colonic cancer by MNNG in rats on a low calcium diet, can be reduced by a calcium enriched diet even in the presence of a low fat intake.

Animals↗

PubMed1985

Effect of hypocalcemia on cardiac function in very-low-birth-weight preterm neonates: studies of blood ionized calcium, echocardiography, and cardiac effect of intravenous calcium therapy.

Traditionally, in infants, a serum calcium value less than 7.0 mg/dL is considered to impair cardiac function. In very-low-birth-weight infants, we studied the hypotheses that decline in serum calcium to 6.0 mg/dL (1) would not impair cardiac function and (2) ionized calcium would remain greater than 3.0 mg/dL. We also evaluated the effect of calcium infusion on cardiac function. We studied 15 normokalemic and normonatremic infants whose birth weights were 822 to 1,450 g and were less than 32 weeks' gestation. When serum calcium declined to less than 6.0 mg/dL, 18 mg/kg of calcium as 5% calcium gluconate was infused for 10 minutes. Serum total calcium concentration, blood ionized calcium concentration, ECG, and M-mode echocardiogram were obtained on entry into the study, when the infants were hypocalcemic, immediately after treatment with calcium, and eight hours after treatment. Ionized calcium values were calculated based on serum total calcium and serum protein, and corrected calcium values were calculated based on serum total calcium, serum albumin, and blood pH. In all infants, serum calcium value declined to less than 7.0 and in eight infants to less than 6.0 mg/dL. Assessment of heart rate, systolic blood pressure, ejection fraction, left ventricular systolic time interval, right ventricular systolic time interval, fiber shortening index, and left ventricular mean velocity of circumferential fiber shortening showed no significant alteration from baseline during hypocalcemia or in association with intravenous slow bolus infusion of 18 mg/kg of calcium.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Proteins↗

PubMed1995

Effects of calcium sensitizers on intracellular calcium handling and myocardial energetics.

Calcium sensitizers may influence myocardial energetics by their action on calcium turnover and on crossbridge behavior. Using a myothermal method, the effects of the Ca2+ sensitizer EMD-53998 on calcium cycling, crossbridge behavior, and myocardial energy turnover were compared with the effects of an increase in extracellular calcium from 1.25 to 7.5 mM and with the effects of the catecholamine isoproterenol. All three inotropic interventions increased isometric force development in right ventricular rabbit papillary muscles. Relaxation time was decreased with isoproterenol, unchanged with high calcium, and increased with EMD 53998. Calcium cycling-related energy consumption, as measured by tension-independent heat, increased by 234% with high calcium, by 439% with isoproterenol, and by 77% with EMD 53998. In contrast to high calcium and isoproterenol, EMD 53998 increased economy of crossbridge cycling by increasing the force-time integral of the individual crossbridge cycle. The data indicate that EMD 53998 acts by phosphodiesterase inhibition and myofilament calcium sensitization. The latter effect is in part mediated by alteration of crossbridge behavior. Because of its effects on calcium cycling and crossbridge function myocardial energy turnover was reduced significantly with EMD 53998, whereas energy turnover was unchanged with high calcium and was increased with isoproterenol. The new calcium sensitizer levosimendan was investigated in isolated failing human myocardium. Levosimendan dose-dependently increased isometric tension. The inotropic effect was associated with increased rate of relaxation and reduced relaxation time. Measurements of intracellular calcium using the photoprotein aequorin suggest that levosimendan acts by increasing myofilament calcium sensitivity and by increasing cAMP due to phosphodiesterase inhibition. However, the contribution of the cAMP system to the action of levosimendan appears to be rather small. Therefore, the finding of a positive lusitropic effect of levosimendan may be consistent with the notion that levosimendan binds to troponin-C and increases calcium sensitivity only at high (systolic) intracellular calcium concentrations.

Adrenergic beta-Agonists↗

PubMed1998

Calcium-PTH relationship in dialysis patients: the pitfalls of using a constant dialysate calcium concentration during the dynamic tests.

The calcium-PTH relationship in uremic patients has been often studied during dialysis sessions with high or low dialysate calcium concentration (CaD). This method has been used because it is less complex and invasive than i.v. infusion of calcium salts and calcium chelating agents. However, the constancy of CaD during the tests does not allow for the control of the serum calcium profile and, given that the blood calcium concentration is only one factor of a more complex calcium-related mechanism of the PTH release, the calcium-PTH curve may become dependent on the unpredictable rate at which the ionized calcium changes. Dynamic testing of the parathyroid gland was performed in 9 dialysis patients comparing constant CaD of 1.0 and 2.0 mmol/l (A) with a linear change in CaD (B). The rate of serum calcium change remained constant over time only in experiment B. The total decrease in calcemia (0-0.38 +/- 0.03 vs -0.14 +/- 0.1 mmol/l) and PTHmax (748.25 +/- 124.76 vs 374.89 +/- 53.03 pg/ml) were significantly higher in B, whereas the total increase in calcemia (+0.26 +/- 0.03 vs +0.28 +/- 0.02 mmol/l) and the minimum value of PTH (59.15 +/- 9.53 vs 55.64 +/- 9.08 pg/ml) were similar in both experiments. The calcium-PTH curves were clearly different in A and B. The setpoint and the slope were significantly higher in A (1.196 +/- 0.01 vs 1.142 +/- 0.02 mmol/l; 840.54 +/- 96.85 vs 542.43 +/- 112.26%/mmol). For similar serum calcium values (1.084 +/- 0.01 vs 1.059 +/- 0.02 in the stimulation test and 1.325 +/- 0.02 vs 1.336 +/- 0.02 mmol/l in the inhibition test) the PTH secretion was significantly different (335.86 +/- 44.36 vs 647.65 +/- 104.09 in the stimulation test and 76.35 +/- 12.57 vs 105.03 +/- 20.59 pg/ml in the inhibition test). In conclusion, the way of inducing serum calcium change affected the calcium-PTH curve and the value of the set point and the slope was a function of the way in which the blood calcium changes were achieved. The modulated CaD dialysis was shown to be a more correct method of studying the calcium-PTH relationship in dialysis patients, as well as an alternative to the more complex and invasive infusional methodology.

Calcium↗

PubMed1997

Acute changes in serum calcium and parathyroid hormone circulating levels induced by the oral intake of five currently available calcium salts in healthy male volunteers.

Several calcium supplements are currently available and many of them are marketed without proper comparison of the bioavailability of the actual preparations. The aim of the present trial was to evaluate and compare the acute changes in serum calcium (Ca) and parathyroid hormone (PTH) levels following the oral administration of a vehicle and of five calcium salts currently prescribed in Western Europe. No significant changes in serum Ca or PTH levels were observed after administration of the vehicle. All calcium salts induced significant increases in serum Ca and decreases in serum PTH compared to baseline values. Comparison of the six response curves revealed a significantly greater increase in serum Ca and a greater decrease in serum PTH after each of the calcium salts than observed after the vehicle. However, no statistically significant differences were observed between the different calcium salts for serum Ca increments. The decrease in serum PTH observed after administration of an ossein-hydroxyapatite complex was significantly less important than after the four other calcium salts, even if statistically different than after vehicle. When assessing the area under the curve (AUC) of PTH values, we observed that calcium carbonate and citrate induce a significantly greater decrease in serum PTH than the other calcium salts which are, however, statistically more active than the vehicle. Serum PTH is decreased under the lower limit of the normal range (10 pg/ml), between t60 and t120 for calcium carbonate and citrate and between t60 and t90 for calcium gluconolactate while the mean PTH values remain within the normal range throughout the study with calcium pidolate, the ossein-hydroxyapatite complex and the vehicle. In conclusion, all calcium preparations significantly increase serum calcium and decrease serum parathormone, compared to what is observed after oral intake of a vehicle. However, significant differences in suppression of parathormone are observed between the different calcium preparations and might be of importance for their clinical use.

Administration, Oral↗

PubMed1990

Effect of pressure and calcium on the reversible inhibition of the sarcoplasmic-reticulum calcium-transport enzyme and on its tryptic cleavage pattern.

The reversible inhibition of the sarcoplasmic-reticulum calcium-transport enzyme by pressure at room temperature is accompanied by a significant enhancement of the accessibility of the enzyme to tryptic cleavage dependent on the presence of calcium. The calcium-transport enzyme activity was monitored with dinitrophenyl phosphate as substrate. Pressure in the range 0.1-100.0 MPa affects trypsin cleavage of the control substrate N-alpha-benzoyl-L-arginine-4-nitroanilide hydrochloride little in the presence and absence of calcium. In contrast, application of 100.0 MPa to the calcium-transport enzyme at room temperature accelerates subsequent tryptic cleavage at the T2 but not at the T1 cleavage site [C. J. Brandl et al. (1986) Cell 44, 597-607]. Pressure application during tryptic digestion likewise solely affects cleavage at T2 which proceeds slowly in the absence but rapidly in the presence of calcium. At atmospheric pressure in the absence of calcium and at high pressure in the absence and presence of calcium new cleavage sites are exposed giving rise to new subfragments B1-3 in addition to the established peptides A1 and A2. Under pressure and in the presence of calcium, A1 and A2 rapidly disappear indicating the presence of calcium-binding sites in these peptides. In contrast, the B1-3 peptides which are most likely derivates of the B fragment accumulate in the presence and absence of calcium. In contrast to tryptic cleavage at atmospheric pressure, tryptic cleavage of the A as well as the B fragment tends to completion under pressure. In parallel to the disappearance of the A and B fragments calcium-dependent substrate hydrolysis vanishes. Computation of activation volumes for pressure-induced reversible enzyme inhibition and for tryptic cleavage furnished closely related volumes of opposite signs of 20-40 ml/mol and 80-100 ml/mol in the ranges 0.1-40.0 MPa and 40.0-100.0 MPa, respectively. Thus pressure produces reversible changes in the calcium-transport enzyme which activates and modifies tryptic-cleavage patterns at the T2 site of the A segment and at sites in its subfragments in the presence of calcium, i.e. if the enzyme residues in its E1 state. In contrast tryptic cleavage of the B fragment is accelerated by pressure independently of the presence of calcium.

Animals↗

PubMed1996

Voltage-dependent calcium currents and cytosolic calcium in equine airway myocytes.

1. The relationship between voltage-dependent calcium channel current (I(Ca)) and cytosolic free calcium concentration ([Ca2+]i) was studied in fura-2 AM-loaded equine tracheal myocytes at 35 degrees C and 1.8 mM Ca2+ using the nystatin patch clamp method. The average cytosolic calcium buffering constant was 77 +/- 3 (n = 14), and the endogenous calcium buffering constant component is likely to be between 15 and 50. 2. I(Ca) did not evoke significant calcium-induced calcium release (CICR) since (i)[Ca2+]i scaled with the integrated I(Ca) over the full voltage range of evoked calcium currents, (ii) increases in [Ca2+]i associated with I(Ca) were consistent with cytoplasmic buffering of calcium ions entering through voltage-dependent calcium channels (VDCCs) only, (iii) there was a fixed instantaneous relationship between transmembrane calcium flux (J(Ca)) and the change in cytosolic free calcium concentration (delta [Ca2+]i) during I(Ca), (iv) caffeine (8 mM) triggered 8-fold higher calcium transients than I(Ca), and (v) I(Ca) evoked following release of intracellular calcium by caffeine resulted in an equivalent delta[Ca2+]i-J(Ca) relationship. 3. The time constant (T) for the decay in [Ca2+]i was 8.6 +/- 1.5 s (n = 8) for single steps and 8.6 +/- 1.1 s (n = 13) following multiple steps that increased [Ca2+]i to much higher levels. Following application of caffeine (8 mM), however, [Ca2+]i decay was enhanced (T = 2.0 +/- 0.2 s, n = 3). The rate of [Ca2+]i decay was not voltage dependent, was not decreased in the absence of extracellular Na+ ions, and no pump current was detected. 4. We conclude that under near physiological conditions, neither CICR nor Na(+)-Ca2+ exchange play a substantial role in the regulation of I(Ca)-induced increases in [Ca2+]i, and that, even following release of intracellular calcium by caffeine, Na(+)-Ca2+ exchange does not play an appreciable role in the removal of calcium ions from the cytosol.

Animals↗

PubMed1999

A calcium antagonist protects against doxorubicin-induced impairment of calcium handling in neonatal rat cardiac myocytes.

The effects of doxorubicin (DOX) on intracellular calcium transients and the cardioprotective effects of a calcium antagonist on DOX-induced impairment of calcium handling were examined in neonatal rat cultured cardiac myocytes. Cultured cardiac myocytes isolated from neonatal Wistar-Kyoto rats were treated with DOX for 24 h. Field-stimulated calcium transients in single myocytes were measured in the presence or absence of isoproterenol using fura-2/AM. Calcium transients were also measured after the addition of DOX to myocytes pretreated with a calcium antagonist, benidipine. DOX reduced the amplitude, maximum velocity of increase and decrease of calcium transients and prolonged the time course of calcium transients and impaired the beta-adrenoceptor responsiveness of calcium transients in a concentration-dependent manner. The DOX-induced impairment of calcium transients and beta-adrenoceptor responsiveness was improved by 10(-8) mol/L of benidipine. However, these improvements decreased with increasing concentrations of benidipine. DOX impaired both the mobilization and removal of intracellular calcium ions in contraction-relaxation cycles and the response of calcium transients to beta-adrenoceptor stimulation. Appropriate concentration of benidipine ameliorated DOX-induced impairment of calcium dynamics, suggesting that benidipine, a long-acting calcium antagonist, has potential clinical usefulness on DOX-induced abnormal calcium handling.

Animals↗

PubMed1987

Calcium chloride versus calcium gluconate: comparison of ionization and cardiovascular effects in children and dogs.

A randomized prospective study in both children and dogs compared ionization of calcium chloride and calcium gluconate. Five conditioned dogs under halothane anesthesia received calcium chloride (4, 8, 12 mg/kg) and calcium gluconate (14, 28, 42 mg/kg) intravenously. Ten children scheduled for burn wound excision and grafting received both calcium chloride (2.5 mg/kg) and calcium gluconate (7.5 mg/kg) injected through a central venous cannula. Ionized calcium was measured at 0, 0.5, 1, 3, 5, and 10 min in the children, and 0, 0.5, 1, 2, 3, 4, 5, 10, 20, and 45 min in the dogs. The authors conclude that equal elemental calcium doses of calcium gluconate (10%) and calcium chloride (10%) (approximately 3:1), injected over the same period of time, are equivalent in their ability to raise [Ca++] during normocalcemic states in children and dogs; the changes in [Ca++] following calcium administration are short-lived (minutes); rapidity of ionization seems to exclude hepatic metabolism as an important factor in the dissociation of calcium gluconate; and equivalent rises in [Ca++] produced by calcium gluconate or calcium chloride resulted in equivalent cardiovascular effects. The authors feel that either form of calcium salt would be satisfactory if indicated during cardiopulmonary resuscitation or for the treatment of ionized hypocalcemia due to massive blood transfusion.

Adolescent↗

PubMed1994

EFFECT OF THE EXTERNAL CONCENTRATION OF CALCIUM ON THE POSTMOULT UPTAKE OF CALCIUM IN BLUE CRABS (CALLINECTES SAPIDUS)

The rate of calcium uptake in blue crabs (Callinectes sapidus Rathbun) acclimated to 2 sea water with a calcium concentration of 1.4 mmol l-1 was dependent on the magnitude and direction of the electrochemical gradient for calcium. When transferred to water with a high calcium concentration (6 mmol l-1), the electrochemical gradient for calcium favoured diffusive influx, and calcium uptake and apparent H+ excretion increased by approximately 50 %. When transferred to water with a low calcium concentration (0.10 mmol l-1), where the electrochemical gradient for calcium strongly favoured diffusive efflux, calcium uptake ceased but apparent H+ excretion continued at a reduced rate. Crabs regulated the free calcium concentration in their blood at approximately 8 mmol l-1 when the external concentration of calcium was 1.4 mmol l-1 or higher, but the concentration of free calcium in the blood decreased to 5.6 and 4.6 mmol l-1, respectively, at external concentrations of calcium of 0.25 and 0.10 mmol l-1. Crabs transferred to water with 0.10 mmol l-1 calcium for the first 2 days after moult accumulated only 2.5 g calcium kg-1 wet mass, about one-quarter of the mass normally accumulated. Seawater-acclimated crabs transferred to 2 salinity at 1 day postmoult took up calcium at a reduced rate, indicating that a period of acclimation is necessary for a component of the active transport system to increase its capacity, for diffusive efflux to be reduced, or for both to occur.

Journal Article↗

PubMed2002

Calcium channel blockers for inhibiting preterm labour.

BACKGROUND: Preterm birth is a major contributor to perinatal mortality and morbidity and affects approximately six to seven per cent of births in developed countries. Tocolytics are drugs used to suppress uterine contractions. The most widely tested tocolytics are betamimetics. Although they have been shown to delay delivery, betamimetics have not been shown to improve perinatal outcome, and they have a high frequency of unpleasant and even fatal maternal side effects. There is growing interest in calcium channel blockers as a potentially effective and well tolerated form of tocolysis. OBJECTIVES: To assess the effects on maternal, fetal and neonatal outcomes of calcium channel blockers, administered as a tocolytic agent, to women in preterm labour. SEARCH STRATEGY: We searched the Cochrane Pregnancy and Childbirth Group's specialised register of controlled trials, the Cochrane Controlled Trials Register (February 2002), MEDLINE, EMBASE, and Current Contents. We also contacted recognised experts and cross referenced relevant material. SELECTION CRITERIA: All published and unpublished randomised trials in which calcium channel blockers were used for tocolysis for women in labour between 20 and 36 weeks gestation. DATA COLLECTION AND ANALYSIS: Standard methods of the Cochrane Collaboration and the Cochrane Pregnancy and Childbirth Group were used. Evaluation of methodological quality and trial data extraction were undertaken independently by three authors. Additional information was sought to enable assessment of methodology and conduct of intention-to-treat analyses. Meta-analysis was conducted assessing the effects of calcium channel blockers compared with any other tocolytic agent. Results are presented using relative risk for categorical data and weighted mean difference for continuous data. MAIN RESULTS: Eleven randomised controlled trials involving 870 women were included. When compared with any other tocolytic agent (mainly betamimetics), calcium channel blockers reduced the number of women giving birth within 48 hours (relative risk (RR) 0.73; 95% confidence interval (CI) 0.54, 0.98) and within seven days (RR 0.76; 95% CI 0.59, 0.99). Calcium channel blockers also reduced the requirement for women to have treatment ceased for adverse drug reaction (RR 0.15; 95% CI 0.06, 0.43), the frequency of neonatal respiratory distress syndrome (RR 0.64; 95% CI 0.45, 0.91) and neonatal jaundice (RR 0.73; 95% CI 0.57, 0.93). REVIEWER'S CONCLUSIONS: When tocolysis is indicated for women in preterm labour, calcium channel blockers are preferable to betamimetic agents. Further research should address the effects of different dosage regimens and formulations of nifedipine on maternal and neonatal outcomes.

Calcium Channel Blockers↗

PubMed1993

Calcium retention and hormone levels in black and white women on high- and low-calcium diets.

Black-white differences in calcium metabolism are sought because they may reveal why blacks have higher bone mass than whites. Comparative studies of calcium absorption in blacks and whites are not available. In this study, we compare fractional calcium retention, an index of calcium absorption, and calcium regulating hormone levels in black and white women on a high-calcium diet and after adaptation to a low-calcium diet. A total of 30 healthy women (15 black and 15 white) had measurements of fractional 47Ca retention and calcium regulating hormone levels after 8 weeks on a 2000 mg calcium diet and, subsequently, after 1, 2, 4, and 8 weeks on a 300 mg calcium diet. By 2 weeks after the diet change, fractional 47Ca retention, parathyroid hormone (PTH), and 1,25-dihydroxyvitamin D [1,25-(OH)2D] had reached a plateau at higher levels, urine calcium at a low level, and serum calcium at the same level (repeated-measures ANOVA). Fractional 47Ca retention, serum calcium, and PTH were similar on both diets in blacks and whites. Blacks had higher levels of 1,25-(OH)2D on both diets (e.g., 125.1 +/- 53.5 SD versus 73.4 +/- 19.0 pmol/liter, P = 0.003 on low-calcium diet) and a greater increase in 1,25-(OH)2D after the diet change (33.9 +/- 30.1 SD versus 11.8 +/- 17.9 pmol/liter, P = 0.021). Serum phosphorus was lower in blacks throughout. For hormone levels and fractional calcium retention to stabilize after a diet change, 2 weeks was needed.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗

PubMed2002

The effects of calcium supplementation to patients with primary hyperparathyroidism and a low calcium intake.

BACKGROUND: In patients with primary hyperparathyroidism (PHPT) a low calcium intake might cause increased bone loss and thus aggravate osteoporosis, and a high intake might increase serum calcium level and the risk of nephrolithiasis. AIM OF THE STUDY: Generally, guidelines recommend a normal calcium intake, and accordingly, those with a low intake might benefit from a modest calcium supplementation. This hypothesis was tested in the present study. METHODS: Thirty-one patients with asymptomatic PHPT were recruited from an epidemiological study (The Tromsø study 1994/95). Those with a daily calcium intake below 450 mg were given calcium supplementation (500 mg Ca(2+)), and those with an intake above 450 mg were followed without supplementation. The study was open and lasted 1 year. Serum levels of calcium, PTH, 25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D, urinary calcium excretion, blood pressure, and bone mineral density (BMD) were measured. RESULTS: Three subjects dropped out without reason, 1 developed abdominal discomfort from the calcium supplementation, and 3 had an increase in serum calcium of more than 0.2 mmol/L and were therefore excluded. The latter three did not differ from the rest of the group at baseline. Of the remaining 24 that completed the study, 17 were given calcium. In this group there was a non-significant increase in serum calcium and urinary calcium excretion, a significant decrease in PTH after 4 weeks (13.2 (6.0) vs 9.4 (3.0) pmol/L, P < 0.05), and a significant increase in BMD at the femoral neck at the end of the study (0.849 (0.139) vs 0.870 (0.153) g/cm(2), P < 0.05). The blood pressure was not significantly affected. CONCLUSIONS: Most patients with mild PHPT and a low calcium intake tolerate a moderate calcium supplement. This may have beneficial effects on the bones, but the patients must be followed carefully.

Aged↗

PubMed2005

The effect of extracellular calcium concentration on calcium-mediated cell signaling in NF1 tumor suppressor-deficient keratinocytes.

Capacitative calcium entry and calcium wave propagation were studied in keratinocytes from healthy volunteers and patients with type 1 neurofibromatosis (NF1) in calcium-depleted and in low calcium culture medium. In previous studies, we found evidence that mutations of the NF1 tumor suppressor gene can lead to altered calcium-mediated cell signaling in keratinocytes cultured in the presence of a high extracellular calcium concentration. The present study demonstrated that the differences between normal and NF1 keratinocytes were dependent on extracellular calcium concentration. Specifically, when keratinocytes were exposed to thapsigargin under calcium-depleted culture conditions the subsequent increase in free intracellular calcium concentration was moderate in NF1 keratinocytes compared to controls. The finding indicates lowered endoplasmic calcium stores in NF1 which may also in part explain the reduced activation signal for capacitative calcium influx and the wound-induced intracellular Ca2+ transient observed in NF1 keratinocytes maintained in culture medium containing 0.05 mM calcium. The differences between control and NF1 keratinocytes were most pronounced when the cells were cultured in the presence of a high (1.8 mM) calcium concentration. Since elevated extracellular calcium levels induce keratinocytes to form cellular contacts and lead to terminal differentiation, markedly aberrant responses of NF1 keratinocytes in the presence of a high calcium concentration may help to explain previous findings on impaired formation of cellular junctions and differentiation in NF1 deficient cells.

Adult↗

PubMed1993

Protective effect of various calcium antagonists against an experimentally induced calcium overload in isolated hepatocytes.

The effect of the hepatotoxic substance diamidinothionaphthene (98/202) on cytosolic, mitochondrial and extra-mitochondrial calcium distribution was measured in isolated rat hepatocytes. The drastic disturbance of the intracellular calcium homeostasis caused by this substance (increase of the cytosolic and mitochondrial calcium contents and depletion of extra-mitochondrial calcium stores, which at last lead to cell death) gave rise to an investigation of the possible cytoprotective effect of calcium antagonists of various chemical classes: verapamil, diltiazem, and nifedipine on isolated hepatocytes. Our results show that all three calcium antagonists prevented cell death caused by 98/202. The 98/202-induced increase of cytosolic and mitochondrial calcium content was inhibited by all three calcium antagonists. However, only verapamil was able to inhibit the depletion of extra-mitochondrial calcium stores. Since 98/202-induced cell death occurs only in the presence of extracellular calcium, it is concluded that calcium antagonists are also able to inhibit the influx of extracellular calcium in liver cells, which leads to a calcium overload of the cytosol and mitochondria. The various ways of interfering with the calcium homeostasis of liver cells qualifies the hepatotoxic substance 98/202 as a suitable in vitro hepatotoxicity model for testing the hepatoprotective effect of different calcium antagonists.

Amidines↗