SEARCH · PubMed Health

Results for “Calcium”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources

PubMed1994

Dietary calcium chloride vs. calcium carbonate reduces urinary pH and phosphorus concentration, improves bone mineralization and depresses kidney calcium level in cats.

The effect of dietary calcium chloride vs. calcium carbonate on mineral metabolism was studied in cats. Ovariectomized cats and female kittens were fed purified diets with a normal calcium level (9.5 mmol Ca/MJ) but containing either calcium carbonate or calcium chloride, or were fed diets with a high calcium level (17.7 mmol Ca/MJ) containing either calcium carbonate alone or equimolar amounts of both calcium carbonate and calcium chloride. A 4 x 4-wk cross-over study using adult cats and a 31-wk parallel study using kittens were conducted. Calcium, phosphorus and magnesium balances were established regularly. In the course of the experiment with the kittens, blood samples were taken and X-ray photographs of the tibiae made. At the age of 39 wk, the kittens were killed, and organs and bones were collected. In both adult cats and kittens fed the high calcium diets, urinary concentrations of magnesium and phosphorus and apparent absorption of these minerals were lower than after feeding the normal calcium diets. Urinary pH and phosphorus concentration were lower in cats and kittens fed diets with calcium chloride instead of calcium carbonate. Body weight gain and tibia growth in the kittens tended to be greater after feeding the diets with calcium chloride. Calcium chloride vs. calcium carbonate and also supplemental calcium chloride in the high calcium diet significantly stimulated femur density and reduced renal calcium concentration.

Aging↗

PubMed1996

Plasma membrane calcium pump-mediated calcium efflux and bulk cytosolic free calcium in cultured aortic smooth muscle cells from spontaneously hypertensive and Wistar-Kyoto normotensives rats.

OBJECTIVE: To compare the efficacy of the calcium pump-mediated calcium efflux pathway in spontaneously hypertensive rats (SHR) with that in Wistar-Kyoto normotensive rats (WKY), at rest and after angiotensin II stimulation. DESIGN: The intracellular free calcium concentration and calcium-45 efflux were measured in parallel, in cultured aortic smooth muscle cells isolated from 10-week-old male SHR and WKY rats. METHODS: The intracellular free calcium concentration and calcium-45 efflux were studied in confluent vascular smooth muscle cells in culture. Experiments were performed in the absence of added extracellular calcium and sodium. Fura-2 was used to measure basal and angiotensin II-stimulated intracellular free calcium concentration. Effluxed calcium-45 was measured over 5s intervals to determine basal and angiotensin II-stimulated calcium efflux rates in SHR and in WKY rats. RESULTS: No significant difference between SHR and WKY rats was observed in basal intracellular free calcium concentration or 100nmol/l angiotensin II-stimulated peak intracellular free calcium concentration. However, significantly elevated basal and 100 nmol/l angiotensin II-stimulated calcium-45 efflux rates were found in SHR. The calcium-45 efflux rates in SHR were elevated when the efflux was normalized with respect to the bulk intracellular free calcium concentration. The time taken to reach the maximum calcium-45 efflux rate after angiotensin II stimulation was reduced in SHR compared with that in WKY rats and was dose-dependent in both rat strains. CONCLUSION: The calcium-pump mediated calcium efflux pathway appears to be more efficient in SHR. This may be the result of post-translational modification, enhanced calcium pump sites in a critical region of the membrane, or the presence of a pool of calcium near the plasma membrane that is not readily detected by cytosolic Fura-2 but is higher in SHR both before and after angiotensin II stimulation.

Animals↗

PubMed2001

Modulation of a voltage-gated calcium channel linked to activation of glutamate receptors and calcium-induced calcium release in the catfish retina.

1. Catfish (Ictalurus punctatus) retinal cone horizontal cells contain an L-type calcium current that has been proposed to be involved in visual processing. Here we report on the modulation of this current by activation of glutamate receptors and calcium-induced calcium release (CICR) from intracellular calcium stores. 2. Fluorescence data obtained from isolated horizontal cells loaded with indo-1 provided evidence of calcium release from an intracellular calcium store sensitive to caffeine, calcium and ryanodine. In the presence of caffeine, ryanodine-sensitive stores released calcium in a transient manner. Release of calcium was blocked when cells were preincubated in BAPTA, in the presence of ruthenium red, or in low concentrations of ryanodine. 3. The release of calcium from ryanodine-sensitive stores directly corresponded with a decrease of the voltage-gated L-type calcium current amplitude. Caffeine-induced modulation of the calcium current was reduced in the presence of ruthenium red. 4. Activation of ionotropic kainate receptors on catfish cone horizontal cells triggered CICR from ryanodine-sensitive stores and mimicked inhibition of the voltage-gated calcium current. Kainate-induced inhibition of the calcium current was diminished when intracellular calcium stores were inhibited with ruthenium red or depleted with ryanodine, or when calmodulin antagonists or CaM kinase II inhibitors were present. 5. These results provide evidence that activation of an ionotropic glutamate receptor on catfish cone horizontal cells is linked to calcium release from ryanodine-sensitive intracellular calcium stores and modulation of the L-type calcium current activity. Inhibition of this calcium current directly or indirectly involves calmodulin and CaM kinase II and represents a possible mechanism used by horizontal cells to affect response properties of these cells.

Animals↗

PubMed1991

Calcium--a neglected key factor in arteriosclerosis. The pathogenic role of arterial calcium overload and its prevention by calcium antagonists.

Using specific calcium antagonists as experimental tools, both the physiological messenger and current carrying function of calcium ions as well as their pathogenetic potencies could be elucidated. Notably, excess intracellular calcium signalling and intra- and extracellular calcium overload turned out to be pathogenetic principles of general importance. In this context, progressive calcium overload of arteriosclerotic vascular walls and the antiarteriosclerotic effects of calcium antagonists, deserve particular interest. In fact, with the help of calcium antagonists, arterial calcium overload as decisive component of various types of experimental arteriosclerosis became accessible to a direct therapeutic intervention. According to their responsiveness to calcium antagonists, two pathophysiologically different types of experimental coronary plaques could be characterized: (1) The calcium type, i.e. coronary calcinosis of vitamin D3-intoxicated rats highly sensitive to calcium antagonist treatment, (2) the cholesterol type, represented by coronary atheromata of cholesterol-intoxicated rabbits; this primary coronary cholesterol accumulation could not be inhibited by calcium antagonists. The formation of conventional human coronary artery plaques is characterized from the very early lesion onwards by a progressive local uptake of calcium, finally leading to lethal consequences. Conversely, the analysis of the mural cholesterol does not allow to discriminate arteriosclerotic from normal coronary artery segments. Thereby, conventional human coronary plaques typically represent a calcium-dominated type of human arteriosclerosis and differ widely from plaques produced in cholesterol-fed rabbits. The results indicate the decisive pathophysiological role of calcium and calcium overload in both calcium-dominated types of experimental arteriosclerosis and conventional human coronary artery plaques. Moreover, the antiarteriosclerotic effects of calcium antagonists are demonstrated to be based--in various types of experimental arteriosclerosis--on the inhibition of intra- and extracellular calcium overload of arterial walls evoked by various risk factors (vitamin D3 intoxication, hypertension, nicotine, diabetes).

Animals↗

PubMed1990

Superior calcium absorption from calcium citrate than calcium carbonate using external forearm counting.

Calcium absorption from calcium citrate was compared with that obtained from calcium carbonate in 20 normal women. It was measured by external forearm counting technique, where the ratio of forearm radioactivity after an oral dose of labeled calcium salt (containing 500 mg calcium) and after an intravenous injection of trace radiocalcium represented fractional calcium absorption. The fractional calcium absorption from calcium citrate was 39.2 +/- 8.6%, which was significantly higher than the 31.2 +/- 9.4% derived from calcium carbonate (p less than 0.001). Seventeen subjects displayed greater calcium absorption from calcium citrate. The remaining three patients, with a lower calcium absorption from the citrate salt, had high levels of calcium absorption from calcium carbonate. It is concluded that calcium is better absorbed from calcium citrate than calcium carbonate when these salts are taken on an empty stomach in most women. The exception might be those with optimum calcium absorption from calcium carbonate.

Absorption↗

PubMed1996

Calcium dependence of calcium extrusion and calcium uptake in mouse pancreatic acinar cells.

1. The droplet technique was used to investigate the calcium dependence of calcium extrusion from pancreatic acinar cells with preserved intracellular environments. The calcium dependence of calcium extrusion indicated a strong co-operativity (Hill coefficient, 3). The half-maximal rate of calcium extrusion occurred at an intracellular free calcium concentration ([Ca2+]i) of approximately 200 nM. At [Ca2+]i levels higher than 400 nM the calcium extrusion mechanism was almost completely saturated. 2. The rate of [Ca2+]i recovery was measured with the same cells under conditions where both calcium extrusion and calcium reuptake occurred simultaneously and under conditions when calcium reuptake was prevented and recovery depended entirely upon calcium extrusion. The rate of [Ca2+]i recovery due to calcium reuptake displayed a very sharp dependence on [Ca2+]i. The rate of [Ca2+]i recovery due to reuptake increased approximately 10 times (from 4.3 to 44.1 nM s-1) for an increase of [Ca2+]i of only 100 nM (from 120 to 220 nM). 3. With a decrease of [Ca2+]i the ratio of rate of calcium extrusion to rate of calcium uptake into internal stores increased, indicating that extrusion plays a more important role at low [Ca2+]i levels. Data for [Ca2+]i recovery rates due to extrusion and due to reuptake allowed us to evaluate the absolute rate of calcium translocation into the internal stores during the recovery process. When [Ca2+]i = 350 nM the total (i.e. bound and free) calcium concentration in the cytosol decreased by approximately 100 microM s-1 due to calcium uptake into internal stores. The rate of uptake was approximately 20 times slower when [Ca2+]i = 120 nM.

Animals↗

PubMed2003

Influence of age, diabetes, and cataract on calcium, lipid-calcium, and protein-calcium relationships in human lenses.

PURPOSE: Calcium is elevated in most cataractous human lenses and may contribute to cataractogenesis. In this study, age-related changes were examined in the total calcium content of clear human lenses and the binding of calcium to lens lipids and proteins. METHODS: Total lens calcium was determined by atomic absorption spectroscopy. Calcium binding was measured by light scattering and measurement of calcium by atomic absorption spectroscopy in bound and unbound fractions. RESULTS: The calcium content of clear human lenses decreased between 18 and 55 years of age and increased between 55 and 75 years, as well as in the presence of cataract. Total calcium levels in clear lenses from subjects with insulin-dependent diabetes did not differ from that in lenses of age-matched control subjects. In vitro binding studies have shown that lens lipids can bind nearly all the calcium present in the human lens. Age and cataract diminished the capacity of lens lipids to bind calcium. Calcium-induced light-scattering, measured in vitro for lens proteins, correlated with increasing age and cataract. CONCLUSIONS: The data support the hypothesis that increased intracellular calcium concentrations and a diminished capacity of lens lipids to bind to calcium initiate a cascade of events that culminates in increased light-scattering from lipids and especially proteins. Calcium binding to lipid membranes cannot directly contribute to light-scattering in cataractous lenses. It has been suggested that most of the diffusible calcium in the lens is in the intercellular spaces and that lens lipids in the outer leaflet of the bilayer bind to that calcium. If so, this could account for the 150-fold difference between free and bound calcium levels in the lens.

Adolescent↗

PubMed2006

Bone calcium turnover during pregnancy and lactation in women with low calcium diets is associated with calcium intake and circulating insulin-like growth factor 1 concentrations.

BACKGROUND: Few data exist on longitudinal changes in bone calcium turnover rates across pregnancy and lactation. OBJECTIVE: Our aim was to characterize calcium kinetic variables and predictors of these changes across pregnancy and early lactation in women with low calcium intakes. DESIGN: Stable calcium isotopes were administered to 10 Brazilian women during early pregnancy (EP; weeks 10-12 of gestation), late pregnancy (LP; weeks 34-36 of gestation), and early lactation (EL; 7-8 wk postpartum). Multicompartmental modeling was used to assess the rates of bone calcium turnover in relation to calcium intakes and circulating concentrations of parathyroid hormone (PTH), insulin-like growth factor 1, and 1,25-dihydroxyvitamin D. RESULTS: Rates of bone calcium deposition increased significantly from EP to LP (P = 0.001) and were significantly associated with serum PTH during LP (P < or = 0.01). Rates of bone calcium resorption were also higher during LP and EL than during EP (P < or = 0.01) and were associated with both PTH (P < or = 0.01) and IGF-1 (P < or = 0.05) during LP but not during EL. Net balance in bone calcium turnover was positively associated with dietary calcium during EP (P < or = 0.01), LP (P < or = 0.01), and EL (P < or = 0.01). The mean (+/-SD) calcium intake was 463 +/- 182 mg/d and, in combination with insulin-like growth factor 1, explained 68-94% of the variability in net bone calcium balance during pregnancy and lactation. CONCLUSIONS: Net deficits in bone calcium balance occurred during pregnancy and lactation. Increased dietary calcium intake was associated with improved calcium balance; therefore, greater calcium intakes may minimize bone loss across pregnancy and lactation in women with habitual intakes of <500 mg calcium/d.

Adult↗

PubMed1999

Meta-analysis of calcium bioavailability: a comparison of calcium citrate with calcium carbonate.

OBJECTIVE: To perform a meta-analysis of data from available published trials comparing the bioavailability of calcium carbonate with that of calcium citrate. DATA SOURCES: The whole set was comprised of 15 studies involving 184 subjects who underwent measurement of calcium absorption from calcium carbonate and calcium citrate. Category A excluded four studies for lack of physiological relevance, use of a mixed preparation with low content of calcium carbonate, or wide variability in results. Category B was comprised of five studies (from Category A) involving 71 subjects who took calcium supplements on an empty stomach. Category C was comprised of six studies (from Category A) involving 65 subjects who took calcium preparations with meals. METHOD: The meta-analysis of calcium absorption data from calcium carbonate and calcium citrate, with calculation of effect size and 95% confidence intervals. RESULTS: Calcium absorption from calcium citrate was consistently significantly higher than that from calcium carbonate by 20.0% in the whole set, by 24.0% in Category A, by 27.2% on an empty stomach, and by 21.6% with meals. CONCLUSION: Calcium citrate is better absorbed than calcium carbonate by approximately 22% to 27%, either on an empty stomach or co-administered with meals.

Biological Availability↗

PubMedDate not supplied

Calcium-induced calcium release and calcium buffering in retinal horizontal cells.

Calcium plays an integral role in intracellular signaling and process control in neurons. In the outer retina, it is a key component to the phototransduction cycle and neurotransmitter release in photoreceptor and bipolar cell terminals. It also contributes to the responses of horizontal and bipolar cells. In the dark, horizontal cells are depolarized and calcium enters via calcium permeant AMPA receptors and voltage-activated calcium channels. As a result, horizontal cells must be capable of handling high calcium loads without sustaining damage. The aim of this study was to examine the components determining the intracellular calcium levels in H2 horizontal cells in the retina of white bass. Calcium responses were evoked in isolated cells by depolarizing voltage steps and monitored by conventional imaging techniques. The responses consisted of two components: calcium entry through voltage-gated calcium channels and subsequent release from intracellular stores by calcium-induced calcium release (CICR). Under control conditions, changes in calcium levels reached 541 nM on average from a basal level of 60 nM. When release from CICR stores was blocked with ryanodine or dantrolene, calcium levels barely reached 180 nM. The threshold level needed to trigger CICR was dependent on the duration of the applied depolarization and increased in response to shorter pulses. In studies of temporal integration, cells were depolarized to 0 mVs for increasing periods of time. In the absence of CICR, the responses grew exponentially with time and saturated at approximately 200 nM in response to pulses of 8 s or longer. CICR extended the range of temporal integration to 20 s and the saturating maximum rose to 600 nM. Our results indicate that the slow time-course of the responses, the relatively small changes in intracellular calcium, and the contribution of CICR are shaped by the activity of strong calcium-removal mechanisms and an unusually large calcium-buffering ratio estimated to be over 2,500.

Animals↗

PubMed2000

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

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

Animals↗

PubMed1975

The role of the parathyroids for the adaptation to a low calcium intake. 4. The long-term effect of parathyroidectomy on the adaptation to a low calcium intake in adult rats with special reference to calcium metabolism.

One-year-old selectively parathyroidectomized rats showed, on a normal dietary intake of calcium, phosphorus and vitamin D, a reduction in plasma calcium to below 4.1 mEq./1 in 86 per cent and on restricted calcium intake in 100 per cent. On the normal level of dietary calcium, normalization of plasma calcium occurred 17 per cent within 8 weeks and in another 40 per cent between the 8th and 27th week of observation while on the low level only 10 per cent of the animals normalized their plasma calcium and first after the long-term period of observation. This was most probably accomplished by successively restored parathyroid activity from aberrant parathyroid tissue as deducted from data regarding the metabolism of calcium, magnesium and inorganic phosphate. Adaptation, viz. normalization of plasma calcium, was brought about by mobilization of skeletal calcium with resulting osteoporosis, as reported in our previous study on the same animals. Intestinal net absorption of calcium showed no significant difference between normocalcemic normophosphatemic intact and hypocalcemic hyperphosphatemic parathyroidectomized animals at the respective level of dietary calcium. Thus, parathyroidectomized animals with persistently reduced plasma calcium showed a normal adaptory increase in intestinal calcium absorption upon chronically restricted calcium intake. In the discussion of the regulation of this adaptory system the possible effects of the plasma concentrations of both calcium and inorganic phosphate upon the intracellular Ca22+concentration in the kidney tubules must be considered. Plasma magnesium did not appear to have a primary influence. Intestinal absorption of inorganic phosphate was not dependent upon the presence of the parathyroids but followed that of calcium suggesting a regulation by the action of 1,25-dihydroxycholecalciferol.

Adaptation, Physiological↗

PubMed2003

Calcium fluxes in human trophoblast (BeWo) cells: calcium channels, calcium-ATPase, and sodium-calcium exchanger expression.

Although placental transfer of maternal calcium (Ca(2+)) is a crucial process for fetal development, the biochemical mechanisms are poorly understood. In the current study, we have investigated the characteristics of Ca(2+) fluxes in relation with cell Ca(2+) homeostasis in the human placental trophoblast cell line BeWo. Time-courses of Ca(2+) uptake by BeWo cells displayed rapid initial entry (initial velocity (V(i)) of 3.42 +/- 0.35 nmol/mg protein/min) and subsequent establishment of a plateau. Ca(2+) efflux studies with (45)Ca(2+)-loaded cells also showed rapid declined of cell-associated (45)Ca(2+) with a V(i) of efflux (Ve(i)) of 3.30 +/- 0.08 nmol/mg protein/min. Further identification of membrane gates for Ca(2+) entry in BeWo cells was carried out. Expression of Ca(2+) transporter/channel CaT1 and L-type alpha(1S) subunit was showed by RT-PCR. However, mRNA for CaT2 channel and L-type alpha(1C) and alpha(1D) subunits were not revealed. Membrane systems responsible for intracellular Ca(2+) extrusion from BeWo cells were also investigated. Plasma membrane Ca(2+)-ATPases (PMCA) and Na/Ca exchangers (NCX) were detected by Western blot in BeWo cells. Expression of specific isoforms of PMCA and NCX was further investigated by RT-PCR. Messenger RNAs of four isoforms of PMCA (PMCA 1-4) were detected. The presence of messenger RNAs of two NCX isoforms (NCX1 and NCX3) was observed. Ca(2+) flux studies in Na-free incubation medium indicated that NCX played a minimal role in the cell Ca(2+) fluxes. Inorganic ions such as cadmium and manganese did not modify the Ca(2+) fluxes, however, barium increased cell-associated (45)Ca(2+) by, in part, by reducing radiolabel exit.

Calcium↗

PubMed2003

Absorbability of calcium from calcium-bound phosphoryl oligosaccharides in comparison with that from various calcium compounds in the rat ligated jejunum loop.

Calcium-bound phosphoryl oligosaccharides (POs-Ca) were prepared from potato starch. Their solubility and in situ absorbability as a calcium source were investigated by comparing with the soluble calcium compounds, calcium chloride and calcium lactate, or insoluble calcium compounds, calcium carbonate and dibasic calcium phosphate. The solubility of POs-Ca was as high as that of calcium chloride and about 3-fold higher than that of calcium lactate. An in situ experiment showed that the intestinal calcium absorption rate of POs-Ca was almost comparable with that of the soluble calcium compounds, and was significantly higher (p<0.05) than that of the insoluble calcium groups. Moreover, the total absorption rate of a 1:1 mixture of the calcium from POs-Ca and a whey mineral complex (WMC) was significantly higher (p<0.05) than that of WMC alone. These results suggest that POs-Ca would be a useful soluble calcium source with relatively high absorption in the intestinal tract.

Animals↗

PubMed2002

Risk of calcium oxalate nephrolithiasis in postmenopausal women supplemented with calcium or combined calcium and estrogen.

BACKGROUND: Recent studies showed that postmenopausal women lost less bone mass when supplemented with calcium or estrogen therapy. However, the safety of the treatments in terms of the risk of calcium oxalate stone formation is unknown. We therefore conducted this study to determine the alteration in calcium oxalate supersaturation after calcium supplement or after combined calcium and estrogen therapy in postmenopausal osteoporotic women. METHODS: Fifty-six postmenopausal women were enrolled in this study. All subjects were more than 10 years postmenopausal with vertebral or femoral osteoporosis by bone mineral density criteria. They were randomly allocated to receive either 625 mg of calcium carbonate (250 mg of elemental calcium) at the end of a meal three times a day (group A, n=26) or calcium carbonate in the same manner plus 0.625 mg/day of conjugated equine estrogen and 5 mg medrogestone acetate from day 1-12 each month (group B, n=30). The age (mean +/- S.E.M.) was 66.3 +/- 1.2 and 65.1 +/- 1.1 years, weight 54.1 +/- 1.2 and 55.3 +/- 2.1 kg, in group A and group B, respectively. Urine specimens (24-h) were collected at baseline and 3 months after treatment for the determination of calcium oxalate saturation by using Tiselius's index (AP(CaOx)) and calcium/citrate ratio. RESULTS: After 3 months of treatment, there was no significant alteration from baseline for urinary excretion of calcium, citrate and oxalate. Urinary phosphate excretion was significantly reduced (6.3 +/- 0.7 vs. 5.1 +/- 0.7 mmol/day for group A and 8.2 +/- 0.9 vs. 5.8 +/- 0.7 mmol/day for group B, P<0.05), whereas net alkaline absorption was significantly elevated (10.1 +/- 3.6 vs. 20.1 +/- 4.4 meq/day for group A and 4.8 +/- 3.2 vs. 19.9 +/- 3.6 meq/day for group B, P<0.05). Calcium/citrate ratio and AP(CaOx) determined at baseline were not different from the corresponding values after treatment in both groups; calcium/citrate: 10.1 +/- 3.1 vs. 10.1 +/- 2.5 for group A and 9.3 +/- 1.8 vs. 11.9 +/- 2.5 for group B and AP(CaOx): 1.1 +/- 0.1 vs. 1.3 +/- 0.2 for group A and 1.2 +/- 0.2 vs. 1.1 +/- 0.1 for group B. There were eight and nine patients with high AP(CaOx), or >2, at baseline and after treatment, respectively. CONCLUSIONS: Calcium supplement with a meal or combined calcium supplement and estrogen therapy is not associated with a significant increased risk of calcium oxalate stone formation in the majority of postmenopausal osteoporotic patients. Determination of urinary saturation for calcium oxalate after calcium and estrogen supplements, especially at the initial phase of treatment, may be helpful in the avoidance of nephrolithiasis.

Aged↗

PubMed2001

Does it make a difference how and when you take your calcium? The acute effects of calcium on calcium and bone metabolism.

BACKGROUND: Calcium supplements are widely used to prevent osteoporosis. However, little is known about the metabolic effects of different dosages and of the timing of the dosages. OBJECTIVE: The aim was to study the effects of the timing of the dose (study 1), the effects of the size of the dose (study 2), and the effects of small repetitive doses (study 3) of calcium on calcium and bone metabolism in women. DESIGN: The investigation was conducted in 3 parts, each with 10 participants. In study 1, calcium loads (0 and 25 mg/kg body wt) were taken at 0900 and 2100. In study 2, calcium loads of 0, 250, and 1000 mg were taken at 0900. In study 3, calcium loads of 0 and 200 mg were taken 4 times/d. Markers of calcium and bone metabolism were followed. RESULTS: There was no significant difference in the response of serum parathyroid hormone (PTH) to the calcium load taken at 0900 and that at 2100. There was a significant dose-response effect of the calcium load on serum ionized calcium (P = 0.00005) and serum PTH (P = 0.0003). Small calcium doses (200 mg) taken 4 times/d kept the PTH secretion at a lower level than during the control day (P = 0.016). None of the doses caused significant changes in the markers of bone formation and resorption measured. CONCLUSIONS: The calcium loads had no significant effect on the markers of bone formation and resorption measured, although even small calcium doses decreased serum PTH and increased serum ionized calcium concentrations rapidly. The effect was similar whether calcium was taken in the morning or in the evening.

Adult↗

PubMed1988

[Intracellular free calcium and plasma calcium in patients with essential hypertension. Is there a correlation between extracellular and intracellular disorders of calcium regulation in essential hypertension?].

Alterations in intracellular free calcium regulation as well as disturbances of extracellular calcium homeostasis have been observed in patients with essential hypertension. It has been hypothesized that a generalized defect of calcium regulation might be of importance in the pathogenesis of essential hypertension. In one hypothesis a primary calcium-deficiency in essential hypertension has been linked to subsequent membrane instability and altered intracellular free calcium concentrations. We therefore investigated the relationship between intracellular free calcium concentrations in platelets and ionized as well as total plasma calcium in patients (n = 38) with essential hypertension and in age-matched normotensive subjects (n = 35). Intracellular free calcium in hypertensive patients was elevated by 13% (p less than 0.05) although there was a wide overlap between the values of the two groups. However, no difference with regard to the ionized or total plasma calcium concentrations could be observed. Total plasma calcium concentration, ionized plasma levels as well as intracellular free calcium were positively correlated (p less than 0.05) with mean arterial blood pressure. No correlation however was found between the extracellular and intracellular calcium compartments. We therefore could not observe a generalized defect of calcium regulation in essential hypertension, and extracellular calcium concentrations do not seem to be related to intracellular calcium derangement in this disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2000

Psoriasis and altered calcium metabolism: downregulated capacitative calcium influx and defective calcium-mediated cell signaling in cultured psoriatic keratinocytes.

Intracellular calcium plays an important part in the regulation of proliferation and differentiation of keratinocytes. Detached from their in vivo environment, cultured psoriatic keratinocytes were investigated by monitoring free intracellular calcium concentration, which was measured using fura-2/AM as a calcium-sensitive probe. The mean increase in intracellular calcium of psoriatic keratinocytes was significantly reduced compared with control keratinocytes when intracellular calcium stores were mobilized from endoplasmic reticulum with thapsigargin. This finding suggests defective capacitative calcium influx of psoriatic cells. Intracellular calcium stores were similar in psoriatic and control keratinocytes, when extracellular calcium was chelated with ethyleneglycol-bis(beta-aminoethyl ether)-N,N,N',N',-tetraacetic acid and intracellular calcium was depleted with thapsigargin. Mechanical wounding of keratinocyte monolayer resulted in a significantly reduced rise in intracellular calcium of psoriatic cells in low (< 0.1 mM) and high (1.8 mM) extracellular calcium suggesting defective intercellular coupling of psoriatic keratinocytes. Blocking of gap-junctions with heptanol in wounded keratinocytes did not affect the intracellular calcium response in psoriatic keratinocytes in contrast to healthy keratinocytes. Adding adenosine triphosphate to culture medium resulted in a more pronounced intracellular calcium increase than thapsigargin in psoriatic keratinocytes, suggesting that inositol triphosphate-mediated, P2-purinergic signaling was enhanced in these cells. Moreover, psoriatic keratinocytes maintained their defective responses up to at least fifth passage suggesting that psoriatic keratinocytes have an inborn error in calcium metabolism, rather than a localized defect in response to altered extracellular calcium gradient observed in vivo.

Adenosine Triphosphate↗