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PubMedDate not supplied

Timing of the calcium intake and effect of calcium deficiency on behaviour and egg laying in captive great tits, Parus major.

The calcium demand of egg-laying birds is much higher than in other vertebrates during reproduction. We showed elsewhere that a low level of calcium availability can greatly affect the eggshell quality and reproduction of free-living passerines. However, there are few data on calcium demand and calcium intake in relation to egg laying and behaviour and egg-laying performance under conditions of calcium shortage in nondomesticated birds. We examined these aspects in an experiment with captive great tits, Parus major, on a diet deficient in calcium, with or without snail shells as an additional calcium source. More than 90% of the calcium intake for egg production took place during the egg-laying period. Females ingested about 1.7 times as much calcium as they deposited in eggshells. Removing the snail shells after the first egg resulted in eggshell defects and interruptions of laying after 1-3 d. Females without snail shells doubled their searching effort and started to burrow in the soil and to eat sand, small stones, and their own eggs. Most calcium was consumed in the evening, probably to supplement the calcium available from the medullary bone with an additional calcium source in the gut during eggshell formation. The results demonstrated that eggshell formation requires accurate timing of the calcium intake and that obtaining sufficient calcium is time-consuming, even in calcium-rich environments. These factors pertaining to calcium intake greatly affect the ability of birds to collect sufficient calcium for eggshell formation in calcium-poor areas.

Animals↗

PubMed1991

The treatment of uraemic hyperphosphataemia with calcium acetate and calcium carbonate: a comparative study.

A comparative study of long-term haemodialysis patients investigated the effects of calcium acetate and calcium carbonate on concentrations of serum phosphate, calcium, and parathyroid hormone. It was demonstrated that both substances led to a significant decrease in phosphate and serum parathyroid hormone. Administration of calcium acetate reduced the serum phosphate concentration in 7 weeks from an initial value of 2.08 +/- 0.53 mmol/l to 1.51 +/- 0.39 mmol/l (P less than 0.01). Following a 1-week wash-out period, calcium carbonate reduced the serum phosphate concentration in the same patients from 1.99 +/- 0.62 mmol/l to 1.34 +/- 0.40 mmol/l (P less than 0.01). Of particular significance, however, is the fact that in relation to daily elementary calcium intake, calcium acetate was a considerably more effective binder of intestinal phosphate than calcium carbonate. During administration of calcium acetate only 1.02 g of elementary calcium were required daily in order to reduce the serum phosphate concentration. The same patients, however, required 1.88 g of elementary calcium during calcium carbonate therapy. Complementary studies investigated the influence of an accompanying calcitriol medication. In this instance, too, calcium acetate was shown to be more effective; although the patients developed hypercalcaemia with calcium acetate, this happened more often with calcium carbonate. In summary it can be said that daily calcium loading of the uraemic organism under calcium acetate therapy is reduced by nearly half as compared to calcium carbonate therapy, and that this can be achieved with the same effective decrease of the serum phosphate concentration.

Acetates↗

PubMed2005

Effects of vitamin K2 administration on calcium balance and bone mass in young rats fed normal or low calcium diet.

OBJECTIVE: The purpose of this study was to examine the effects of vitamin K2 administration on calcium balance and bone mass in young rats fed a normal or low calcium diet. METHODS: Forty female Sprague-Dawley rats, 6 weeks of age, were randomized by stratified weight method into four groups with 10 rats in each group: 0.5% (normal) calcium diet, 0.1% (low) calcium diet, 0.5% calcium diet + vitamin K2 (menatetrenone, 30 mg/100 g chow diet), and 0.1% calcium diet + vitamin K2. After 10 weeks of feeding, serum calcium and calciotropic hormone levels were measured, and intestinal calcium absorption and renal calcium reabsorption were evaluated. Bone histomorphometric analyses were performed on cortical bone of the tibial shaft and cancellous bone of the proximal tibia. RESULTS: Feeding a low calcium diet induced hypocalcemia, increased serum parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D [1,25(OH)2D] levels with decreased serum 25-hydrovyvitamin D [25(OH)D] level, stimulated intestinal calcium absorption and renal calcium reabsorption, and reduced cortical bone mass as a result of decreased periosteal bone gain and enlarged marrow cavity, but did not significantly influence cancellous bone mass. Vitamin K2 administration in rats fed a low calcium diet stimulated renal calcium reabsorption, retarded the abnormal elevation of serum PTH level, increased cancellous bone mass, and retarded cortical bone loss, while vitamin K2 administration in rats fed a normal calcium diet stimulated intestinal calcium absorption by increasing serum 1,25(OH)2D level, and increased cortical bone mass. CONCLUSION: This study clearly shows the differential response of calcium balance and bone mass to vitamin K2 administration in rats fed a normal or low calcium diet.

Animals↗

PubMed1987

Calcium ionophore (A23187)- and arachidonic acid-stimulated prostaglandin release from microvascular endothelial cells: effects of calcium antagonists and calmodulin inhibitors.

Calcium ionophore (A23187)-stimulated prostaglandin (PG) E2 and I2 (measured as 6-keto PGF1 alpha) release from cultured rabbit coronary microvessel endothelial (RCME) cells in a time- and dose-dependent manner. A23187-stimulated PG release was reduced by the calcium channel blockers nifedipine, verapamil and diltiazem and by the intracellular calcium blocker, 8-(diethylamino)-octyl-3,4,5-trimethoxybenzoate. A23187-stimulated PG release was significantly reduced by lowering the calcium concentration in the buffer to concentrations of 0.2 mM or less. A23187-stimulated 45Ca uptake was not inhibited by nifedipine (0.5 microM), diltiazem (10 micron) or verapamil (50 microM) although these same concentrations of calcium channel blockers significantly inhibited A23187-stimulated PG release. However, these concentrations of calcium blockers did inhibit K+ (10 mM)-valinomycin (5 microM)-stimulated 45Ca uptake, indicating that, although RCME cells probably have voltage-dependent calcium channels and although calcium influx via these channels is blocked by the calcium channel blockers, voltage-dependent calcium influx plays little or no role in A23187-stimulated 45Ca influx and PG release. KCl-valinomycin significantly stimulated PG release, but this increase was not significantly affected by either nifedipine (0.5 microM) or diltiazem (10 microM) despite complete inhibition of KCl-valinomycin-stimulated 45Ca influx. Verapamil (50 microM) exhibited a small but significant suppression of KCl-valinomycin-stimulated PG release. These observations most likely indicate that calcium influx by voltage-dependent calcium channels plays little or no role in the events leading to either A23187- or KCl-valinomycin-stimulated PG release. The calmodulin antagonists, trifluoperazine and calmidazolium, also reduced A23187-stimulated PG release. In vitro studies of porcine pancreatic phospholipase (PL) A2 activity suggested that the inhibitory actions of trifluoperazine, but not the calcium antagonists, may be mediated by direct inhibitory actions on PLA2. Studies with [3H]arachidonic acid (AA)- and [14C]stearic acid-prelabeled RCME cells suggested that A23187 stimulated both PLA2 and PLC activity, leading to the release of AA. Studies with exogenous AA indicated that reducing calcium availability by reducing buffer calcium concentrations resulted in an enhanced conversion of exogenous AA to PGs. RCME cells incubated in nominally calcium-free buffer exhibited a decreased rate of AA incorporation. The observed increase in AA conversion to PGs in low calcium buffer suggests that calcium may stimulate AA uptake and acylation as well as AA release.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1985

External calcium inhibits the efflux of calcium from isolated retinal rod outer segment disks.

Increasing the concentration of calcium in the external buffer flowing past isolated, intact bovine retinal rod outer segment disks immobilized in a flow system reduced the rate of radioactive calcium efflux from within the disks in the dark. We interpret these results as extradiskal calcium acting at an inhibitory binding site to block the calcium efflux. A Scatchard analysis of the external calcium dependence of the efflux yields an apparent dissociation constant of 50 microM, which further suggests that the inhibition is mediated by a specific membrane binding site. The observed inhibition of calcium efflux may represent a functional role for the high-affinity calcium binding site which has been identified by others in previous physical studies of the disk membrane. This external calcium inhibited permeability may explain some of the discrepancies in the reported calcium transport properties of disks. Variations in the external calcium concentration may alter the calcium content of isolated disks, thereby indirectly affecting other transport functions including the measured light-induced release of calcium. No evidence was found for either Na/Ca or Ca/Ca exchange processes across the disk membrane. Lanthanum was even more effective than calcium in inhibiting calcium efflux in the dark. Neither lanthanum nor calcium inhibited the light-induced efflux of calcium from disks, which implies either that light and extradiskal calcium regulate separate permeability processes in the disk membrane or that light greatly reduces the affinity of the inhibitory site for calcium and lanthanum.

Animals↗

PubMed1987

Extra calcium on shortening in barnacle muscle. Is the decrease in calcium binding related to decreased cross-bridge attachment, force, or length?

Barnacle single muscle fibers were microinjected with the calcium-specific photoprotein aequorin. We have previously shown (Ridgway, E. B., and A. M. Gordon, 1984, Journal of General Physiology, 83:75-104) that when barnacle fibers are stimulated under voltage clamp and length control and allowed to shorten during the declining phase of the calcium transient, extra myoplasmic calcium is observed. The time course of the extra calcium for shortening steps at different times during the calcium transient is intermediate between those of free calcium and muscle force. Furthermore, the amplitude increases with an increased stimulus, calcium transient, and force. Therefore, the extra calcium probably comes from the activating sites on the myofilaments, possibly as a result of changes in calcium binding by the activating sites. The change in calcium binding may be due, in turn, to the change in muscle length and/or muscle force and/or cross-bridge attachment per se. In the present article, we show that the amount of the extra calcium depends on the initial muscle length, declining at shorter lengths. This suggests length-dependent calcium binding. The relation between initial length and extra calcium, however, parallels that between initial length and peak active force. The ratio of extra calcium to active force is therefore virtually independent of initial length. These data do not distinguish between a direct effect of length on calcium binding and an indirect effect owing to changes in cross-bridge attachment and force through some geometrical factor. The amount of extra calcium increases with the size of the shortening step, tending toward saturation for steps of greater than or equal to 10%. This experiment suggests that calcium binding depends on muscle force or cross-bridge attachment, not just length (if at all). There is much less extra calcium seen with shortening steps at high force when the high force results from stretch of the active muscle than when it results from increased stimulation of muscle.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1997

Calcium retention in relation to calcium intake and postmenarcheal age in adolescent females.

Achievement of maximal calcium retention during adolescence may influence the magnitude of peak bone mass and subsequently lower the risk of osteoporosis. Calcium retention is generally considered to reach a plateau at a certain calcium intake. To test this hypothesis, calcium balance was measured in 35 females with a mean (+/-SD) age of 12.7 +/- 1.2 y (range: 12-15 y) who consumed from 841 +/- 153 to 2173 +/- 149 mg Ca/d. Subjects ate a basal diet that included a fortified beverage containing different amounts of calcium citrate malate. Twenty-one subjects were studied at two dietary calcium intakes with use of a crossover design. Results from a previous study in 14 subjects who were studied at only one calcium intake were included in the data analysis. Calcium retention was modeled as a nonlinear function of calcium intake that included a parameter representing mean maximal retention. Mean maximal calcium retention was 473 mg/d (95% CI: 245, 701 mg Ca/d). At higher postmenarcheal ages, maximal calcium retention was lower but the intake required to achieve this was not affected. Calcium intake explained 79% and 6%, respectively, of the variation in fecal and urinary calcium excretion. Intake of 1200 mg Ca/d, the recommended dietary allowance for calcium published in 1989, resulted in a mean calcium retention that was 57% of the maximal value (95% CI: 25%, 89%). Intake of 1300 mg Ca/d was the smallest intake that allowed some adolescent females to achieve 100% of maximal calcium retention (95% CI: 26%, 100%). These data support the idea that calcium retention plateaus at a certain calcium intake although it continues to increase at intakes > 2 g/d.

Adolescent↗

PubMed1992

Calcium absorption and calcium bioavailability.

Calcium is important for bone health. It has been customary to focus on dietary calcium intake, but of central importance for the body needs in the individual patient is the actual calcium absorption. This absorption consists of an active vitamin D-mediated component and a passive diffusional component. A number of different methods are available for the evaluation of calcium absorption. At present the calcium absorption tests using calcium isotopes (radioactive or stable) appear to be the most reproducible way of determining calcium absorption. The major nutrient sources for calcium are milk and milk products, whereas some of the green vegetables have a low bioavailability of calcium. When deciding whether an increased calcium intake is advisable, the following questions must be answered. What is the calcium absorptive status of the patient? How should the calcium supplement be dispensed? What calcium salt should be used? When should calcium supplements be taken? What is the compliance of the patient? When should the treatment be evaluated? The calcium supplement might be taken as milk (or milk products) or, in patients with lactose intolerance, as calcium supplements. Quite a number of calcium supplements are available on the market, and many of them are marketed without proper knowledge of the bioavailability of the actual preparation. For the benefit of our patients it is now reasonable to demand such investigations before marketing calcium supplements.

Biological Availability↗

PubMed1996

Calcium deficiency in fluoride-treated osteoporotic patients despite calcium supplementation.

To test the hypothesis that the osteogenic response to fluoride can increase the skeletal requirement for calcium, resulting in a general state of calcium deficiency and secondary hyperparathyroidism, we assessed calcium deficiency, spinal bone density, by quantitative computed tomography, and serum PTH in three groups of osteoporotic subjects. Two of the three groups had been treated with fluoride and calcium (at least 1500 mg/day) for 32 +/- 19 months. Group 1 consisted of 16 fluoride-treated subjects who had shown rapid increases in spinal bone density (+ 3.8 +/- 2.6 mg/cm2 month), group II consisted of 10 fluoride-treated subjects who had shown decreases or only slow increases in spinal bone density (-0.05 +/- 0.6 mg/cm3 month), and group III consisted of 10 age-matched untreated osteoporotic controls. Calcium deficiency was assessed by measurement of calcium retention after calcium infusion. The results of our studies showed that 1) 94% of the subjects in Group I were calcium deficient compared with only 30% in groups II and III (P < 0.01 for each); 2) the subjects in group I retained more calcium (79%) than the subjects in group II (60%, P < 0.001) or the subjects in group III (64%, P < 0.005); 3) calcium retention was proportional to serum PTH (r = 0.37, n = 36, P < 0.03); and 4) calcium retention was proportional to the (previous) fluoride-dependent increase in quantitative computed tomography spinal bone density (in groups I and II, r = 0.48, n = 26, P < 0.02). To test the hypothesis that the calcium deficiency and the secondary hyperparathyroidism that were associated with the positive response to fluoride would respond to concomitant calcitriol treatment, a subgroup of 7 calcium-deficient subjects were selected from group I and treated with calcitriol (plus fluoride and calcium) for an average of 7 months. The calcitriol therapy reduced the calcium deficit in all 7 subjects, decreasing calcium retention from 80% to 62% (P < 0.02), and decreasing PTH from 50 to 28 pg/mL (P < 0.02). Together, these data indicate that fluoride-treated osteoporotic subjects may develop calcium deficiency in proportion to the effect of fluoride to increase bone formation, and this calcium deficit is responsive to calcitriol therapy.

Aged↗

PubMedDate not supplied

Modulation by ryanodine of active calcium loading and caffeine induced calcium release of heavy sarcoplasmic reticulum vesicles.

The effect of ATP on the calcium release channel in heavy sarcoplasmic reticulum vesicles modulated by ryanodine has been analyzed by monitoring active calcium uptake and caffeine induced calcium release under near physiological conditions. Native as well as ryanodine reacted vesicles display a complex time course of calcium uptake resulting in nearly complete exhaustion of medium calcium when ATP in combination with an ATP-regenerating system, in contrast to ATP alone, or dinitrophenyl phosphate, were used to support calcium uptake. Applying of dinitrophenyl phosphate as energy yielding substrate, not affecting channel activity, allowed to estimate the fraction of light vesicles devoided of calcium channels contaminating the heavy preparation as the fraction that stores calcium after the preparation has been treated with channel opening, low concentrations of ryanodine (1 microM). Calcium uptake by contaminant light vesicles (25%) cannot account for calcium storage, as well as, abolition of caffeine induced calcium release of ryanodine treated heavy vesicles. Calcium uptake of native and ryanodine treated vesicles is accompanied by the uptake of equivalent amounts of inorganic phosphate arising from ATP hydrolysis indicating that calcium is mainly stored as calcium phosphate. The momentary capability of the preparation to accumulate calcium was measured by activating calcium uptake during the calcium storage period with 0.2 mM 45CaCl2 and 4 mM phosphate at short time intervals. A significant increase of the momentary uptake activity with time was observed being more pronounced for ryanodine treated than for native vesicles indicating that under regenerating conditions, ATP can induce closing of the native and even more effectively of the ryanodine modified calcium release channels.

Adenosine Triphosphate↗

PubMed2000

Low fractional calcium absorption increases the risk for hip fracture in women with low calcium intake. Study of Osteoporotic Fractures Research Group.

BACKGROUND: Decreased ability to absorb calcium with age limits adaptation to low calcium intake and is thought to lead to secondary hyperparathyroidism and increased risk for hip and other fractures. However, the associations between fractional calcium absorption, dietary calcium intake, and risk for fracture have never been studied. OBJECTIVE: To determine whether low fractional calcium absorption in women with low calcium intake increases the risk for subsequent hip and other nonspine fractures. DESIGN: Prospective cohort study. SETTING: Four clinical centers in Baltimore County, Maryland; Portland, Oregon; Minneapolis, Minnesota; and the Monongahela Valley, Pennsylvania. PARTICIPANTS: 5452 nonblack women 69 years of age or older participating in the fourth examination of the Study of Osteoporotic Fractures. MEASUREMENTS: Fractional calcium absorption was measured by using a 3-hour single isotope (45Ca) technique. Incident fractures were identified prospectively and were confirmed by radiographic report. RESULTS: During an average of 4.8 years, 729 women (13%) experienced at least one nonspine fracture; 153 of these women had hip fractures. After adjustment for age, women with lower fractional calcium absorption were at increased risk for hip fracture (relative risk per 1-SD [7.7%] decrease in fractional calcium absorption, 1.24 [95% CI, 1.05 to 1.48]). Women with low fractional calcium absorption and low calcium intake were at greatest risk for subsequent hip fracture; among women whose dietary calcium intake was less than 400 mg/d, those who had fractional calcium absorption at or below the median value of 32.3% had a 2.5-fold (CI, 1.29-fold to 4.69-fold) increase in risk for hip fracture compared with those who had greater absorption efficiency. Fractional calcium absorption was not related to risk for other nonspine fractures (relative risk per 1-SD [7.7%] decrease in fractional calcium absorption, 1.05 [CI, 0.96 to 1.14]). CONCLUSIONS: In elderly women, low fractional calcium absorption in the setting of low calcium intake increases the risk for hip fracture. Our findings support the hypothesis of type II osteoporosis, which postulates that decreased calcium absorption is an important risk factor for hip fracture in older persons.

Aged↗

PubMed1989

[Characterization of calcium permeability at steady-state calcium load in masseter muscle sarcoplasmic reticulum].

To characterize the route of calcium permeability, the effect of intravesicular and extravesicular calcium concentration on the permeability from sarcoplasmic reticulum (SR) vesicles isolated from canine masseter muscle was determined by measuring net efflux of calcium after stopping pump-mediated fluxes. The apparent permeability, calculated as the net efflux divided by the total intravesicular calcium, depended on calcium load. When the intravesicular bound calcium was taken into account, net calcium efflux was found to be linearly related to the difference in calcium concentration across the SR membrane. The first order rate constant of calcium permeability was nearly identical when efflux was initiated by the addition of EGTA or glucose plus hexokinase to quench calcium pump by lowering activator calcium or by converting substrate ATP to ADP and glucose 6-phosphate, respectively. Extravesicular calcium concentration between 0.001 microM and 33.9 microM had no great effect on calcium permeability. The results suggest that some minimal calcium gradient may be required in order to observe a substantial passive calcium efflux, and the passive calcium efflux is not carrier mediated. It is also postulated that passive route of efflux during calcium accumulation is relatively small and that physiological calcium release during excitation-contraction coupling does not occur through this route.

Animals↗

PubMed1996

5-Hydroxytryptamine4 receptors reduce afterhyperpolarization in hippocampus by inhibiting calcium-induced calcium release.

Serotonin acting on 5-hydroxytryptamine4 receptors increases membrane excitability in CA1 hippocampal pyramidal cells by reducing the slow calcium-activated afterhyperpolarization. This effect is mediated through an increase in cAMP and activation of protein kinase A, although subsequent steps have not been elucidated. We now report that a significant portion of the calcium responsible for the generation of the afterhyperpolarization originates from the release of intracellular calcium through a calcium-induced calcium-release mechanism. Thus, the afterhyperpolarization is enhanced by caffeine, whereas it is inhibited by dantrolene and ruthenium red, two blockers of calcium-induced calcium release. The afterhyperpolarization is also inhibited by thapsigargin, which depletes intracellular calcium stores. These observations raised the possibility that serotonin might reduce the afterhyperpolarization by regulating calcium-induced calcium release. Consistent with this possibility, administration of calcium-induced calcium-release blockers, as well as of thapsigargin, occluded the ability of serotonin to inhibit the afterhyperpolarization. Similarly, administration of caffeine, which enhances the contribution of calcium-induced calcium release to the afterhyperpolarization, enhanced the effect of serotonin. These results indicate that serotonin inhibits the afterhyperpolarization in the CA1 region of hippocampus by reducing the ability of extracellular calcium to trigger calcium release from intracellular stores. As such, they identify a physiological role for the calcium-induced calcium release in hippocampus and provide evidence for its regulation by G protein-coupled receptors and, more specifically, 5-hydroxytryptamine4 receptors.

Action Potentials↗

PubMedDate not supplied

[A comparison of phosphorus-chelating effect of calcium carbonate versus calcium acetate before dialysis].

INTRODUCTION: The hyperphosphatemia, hypocalcemia and low calcitriol levels are pathogenic factors for secondary hyperparathyroidism in chronic renal failure. The phosphorus control is essential to prevent secondary hyperparathyroidism. There are not comparatives studies to test the efficacy of control of phosphorus binders in predialysis patients. AIM: To compare the efficacy of calcium carbonate vs calcium acetate as phosphate binder in predialysis patients. MATERIAL AND METHODS: The present study includes 28 patients with chronic renal failure (mean clearance of creatinine 21 ml/min). Patients were separated into two groups: Group 1: (n = 14) received calcium carbonate 2,500 mg/day (1,000 mg of calcium); Group 2: (n = 14) receives calcium acetate 1,000 mg (254 mg of calcium). Calcium and phosphorus were determined every 4 months; i-PTH, alkaline phosphatase and clearance of creatinine were determined every six months. RESULTS: Both groups were comparable regarding age, renal function, calcium, phosphorus, alkaline phosphatase and i-PTH on basal situation and the end of study were not different. The serum calcium increased, not significantly, in the calcium carbonate group (group 1) [from 9.2 to 9.8 mg/dl (p = 0.05)], however it was not modified in the calcium acetate group (group 2). The serum phosphorus decreased significantly (p < 0.05) in both groups, independently of the calcium levels. Alkaline phosphatase and i-PTH not was modified during the study period. CONCLUSIONS: 1) Both calcium carbonate and calcium acetate are similarly effective as phosphate binder. 2) The carbonate group required four fold greater doses of calcium that acetate group. 3) The calcium acetate has less hypercalcemic effect than calcium carbonate.

Acetates↗

PubMed2002

Use of stable calcium isotopes (42Ca & 44Ca) in evaluation of calcium absorption in Beijing adolescents with low vitamin D status.

Female adolescent populations with low calcium intakes and sub-optimal vitamin D status are found in northern China. Whether these individuals are able to adapt by enhancing calcium absorption and reducing calcium excretion for maximizing calcium retention is unknown. This study examined the association between true-fractional-calcium-absorption (TFCA), plasma 25-hydroxy-vitamin-D, and urinary calcium excretion among adolescents in Northern China. Twelve healthy girls 9 to 17 years old were recruited from Beijing during a winter. Calcium intake, anthropometry, pubertal status, plasma 25-hydroxyvitamin-Ds (25-OHD), serum calcium, and urinary calcium were determined. TFCA was evaluated by dual stable calcium isotopes. The mean +/- SD calcium intake, 24-hour urinary calcium excretion, plasma 25-OHD and TFCA were 591 +/- 164 mg/day, 79.9 +/- 49.6 mg/day, 30.5 +/- 9.8 nmol/L, and 60.4 +/- 14.4%, respectively. TFCA was inversely correlated with 25-OHD (r = -0.73, p = .008). Urinary calcium was correlated with the onset of menarche (r = 0.63, p = .027). Post-menarcheal girls had a higher urinary calcium output than premenarcheal girls (p = .03). Adolescents from north China with sub-optimal vitamin-D status are able to adapt by enhancing TFCA and reducing urinary calcium excretion to retain calcium for bone development. TFCA was inversely correlated with plasma 25-OHD. Whether a higher efficiency of calcium absorption is sustainable if the shortfall of vitamin D persisting remains to be studied.

Adolescent↗

PubMed2000

Calcium antagonists for aneurysmal subarachnoid haemorrhage.

BACKGROUND: Rupture of an intracranial aneurysm causes bleeding into the subarachnoid space, which may lead to spasm of the cerebral arteries and ischaemic damage to the brain. Prophylactic use of calcium antagonists in patients with ruptured intracranial aneurysms might reduce the risk of ischaemic damage. OBJECTIVES: This review aimed to determine whether calcium antagonists improve outcome in patients with aneurysmal subarachnoid haemorrhage (SAH). SEARCH STRATEGY: The Cochrane Stroke Group trials register (last searched: March 1999) plus hand searching and personal contacts with trialists and pharmaceutical companies marketing calcium antagonists. SELECTION CRITERIA: All completed, unconfounded, truly randomised controlled trials comparing any calcium antagonist with control, within ten days of SAH onset. Eleven trials that met the inclusion criteria were included in the overview. DATA COLLECTION AND ANALYSIS: Two reviewers independently extracted data and assessed trial quality. Trialists were contacted to obtain missing information. MAIN RESULTS: We analysed 11 trials totalling 2804 randomized patients with subarachnoid haemorrhage (1376 in the treatment and 1428 in the control group). The drugs analyzed were: nimodipine (eight trials, 1574 patients), nicardipine (two trials, 954 patients), and AT877 (one trial, 276 patients). In 92% of the patients aneurysms were confirmed by angiography or autopsy. Overall, calcium antagonists significantly reduce the risk of poor outcome after subarachnoid haemorrhage: relative risk (RR) 0.82 (95% CI 0. 72-0.93); the absolute risk reduction was 5.1%, the corresponding number of patients needed to treat to prevent a single poor outcome event is 20. For oral nimodipine alone the RR was 0.69 (0.58-0.84). The RR of death on treatment with calcium antagonists was 0.94 (95% CI 0.80-1.10), that of ischaemic neurological deficits 0.67 (95% CI 0.59-0.76), and that of CT-scan documented cerebral infarction 0.80 (95% CI 0.71-0.89). REVIEWER'S CONCLUSIONS: Calcium antagonists reduce the proportion of patients with poor outcome and ischemic neurological deficits after aneurysmal SAH; the risk reduction for case fatality alone is not statistically significant. The results for 'poor outcome' are statistically robust, but depend mainly on trials with oral nimodipine; the evidence for nicardipine and AT877 is inconclusive. The intermediate factors through which nimodipine exerts its beneficial effect after aneurysmal SAH remain uncertain.

Calcium Channel Blockers↗

PubMed1998

The calcium sensitivity of individual secretory vesicles is invariant with the rate of calcium delivery.

Differences in the calcium sensitivity of individual secretory vesicles can explain a defining feature of calcium-regulated exocytosis, a graded response to calcium. The role of the time dependence of calcium delivery in defining the observed differences in the calcium sensitivity of sea urchin egg secretory vesicles in vitro was examined. The calcium sensitivity of individual secretory vesicles (i.e., the distribution of calcium thresholds) is invariant over a range of calcium delivery rates from faster than micromolar per millisecond to slower than micromolar per second. Any specific calcium concentration above threshold triggers subpopulations of vesicles to fuse, and the size of these subpopulations is independent of the time course required to reach that calcium concentration. All evidence supports the hypothesis that the magnitude of the free calcium is the single controlling variable that determines the fraction of vesicles that fuse, and that this fraction is established before the application of calcium. Submaximal responses to calcium cannot be attributed to alterations in the calcium sensitivity of individual secretory vesicles arising from the temporal properties of the calcium delivery. Models that attempt to explain the cessation of fusion using changes in the distribution of calcium thresholds arising from the rate of calcium delivery and/or adaptation are not applicable to this system, and thus cannot be general.

Animals↗

PubMed1979

Effects of dietary calcium on blood and tissue lipids, tissue phospholipids, calcium and magnesium levels in rabbits fed diets containing beef tallow.

Levels of lipids, calcium and magnesium in blood and tissue were examined in rabbits to determine the effects of 20% beef tallow diets containing three levels of calcium, less than 0.02, 0.8 or 1.6%. In plasma, the calcium-deficient (less than 0.02%) diet contributed to elevated cholesterol and phospholipid, but had no effect on triglyceride levels. Plasma calcium decreased in the calcium-deficient group and plasma magnesium decreased in the high-calcium (1.6%) group of rabbits. Lipid levels of some tissues varied with the level of dietary calcium. Cholesterol, total phospholipid, sphingomyelin and phosphatidylethanolamine were generally elevated in livers of calcium-deficient rabbits, but the individual phospholipids were decreased in skeletal muscle. Lungs of the calcium-deficient group also had lower phospholipid levels than the high-calcium group. Liver, kidneys, brain and adipose tissue triglyceride levels were highest in the high-calcium group. The calcium level of skeletal muscle was lower in the calcium-deficient group than in the high-calcium group. Calcium in brain and adipose tissue were highest in the calcium-deficient group. Except for adipose tissue, magnesium levels of the tissues studied were not affected by dietary calcium.

Animals↗