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PubMed1985

Calcium bioavailability from calcium carbonate and calcium citrate.

Fourteen normal subjects took 1000 mg calcium orally as calcium citrate or calcium carbonate. The amount of calcium absorbed was estimated from the rise in urinary calcium. The urinary calcium following calcium citrate load significantly higher (by 20-66%), whether expressed as the total amount or as the increment above basal (fasting) excretion. Thus, calcium citrate provides a more optimum calcium bioavailability than calcium carbonate.

Administration, Oral↗
PubMed2006

Serum calcium, urine calcium and polymorphisms of the calcium sensing receptor gene.

BACKGROUND: Recent studies have suggested a correlation between the A986S polymorphism of the calcium sensing receptor (CASR), and serum total and ionized calcium. This study aimed to assess the prevalence of three CASR polymorphisms in a West of Scotland population and relate genotype to serum and urine calcium levels. METHODS: Fasting blood and urine samples were obtained from 121 healthy male and female volunteers aged 20-60 years. Volunteers were genotyped for the A986S, Q1011E and R990G polymorphisms using allele-specific amplification and amplification-created restriction site techniques. Total calcium, ionized calcium and urine calcium excretion were measured using automated clinical chemistry analysers. RESULTS: Genotype frequencies for the A986S polymorphism were: AA, 74.4%; AS, 24.8%; SS, 0.8%. There was a small but statistically significant (P < 0.01) increase in ionized calcium concentration in AS individuals compared with the wild type (1.22 versus 1.20 mmol/L). No statistical difference was detected in serum total calcium or parameters of urine calcium excretion. Genotype frequencies for the remaining polymorphisms were: RR, 82.6%; RG, 16.5%; GG, 0.8% and QQ, 93.4%; QE, 6.6%; EE, 0%. Biochemical parameters in these individuals were not statistically different from the wild type. CONCLUSION: The increase in serum ionized calcium in the AS group was small and, therefore, unlikely to be of clinical significance.

Adult↗
PubMed2000

Mechanisms of calcium decay kinetics in hippocampal spines: role of spine calcium pumps and calcium diffusion through the spine neck in biochemical compartmentalization.

Dendritic spines receive most excitatory inputs in the CNS and compartmentalize calcium. Although the mechanisms of calcium influx into spines have been explored, it is unknown what determines the calcium decay kinetics in spines. With two-photon microscopy we investigate action potential-induced calcium dynamics in spines from rat CA1 pyramidal neurons in slices. The [Ca(2+)](i) in most spines shows two decay kinetics: an initial fast component, during which [Ca(2+)](i) in spines decays to dendritic levels, followed by a slower decay phase in which the spine follows dendritic kinetics. The correlation between [Ca(2+)](i) in spine and dendrite at the breakpoint of the decay kinetics demonstrates diffusional equilibration between spine and dendrite during the slower component. To explain the faster initial decay, we rule out saturation or kinetic effects of endogenous or exogenous buffers and focus instead on (1) active calcium extrusion and (2) buffered diffusion of calcium from spine to dendrite. The presence of an undershoot in most spines indicates that extrusion mechanisms can be intrinsic to the spine. Supporting the two mechanisms, pharmacological blockade of smooth endoplasmic reticulum calcium (SERCA) pumps and the length of the spine neck affect spine decay kinetics. Using a mathematical model, we find that the contribution of calcium pumps and diffusion varies from spine to spine. We conclude that dendritic spines have calcium pumps and that their density and kinetics, together with the morphology of the spine neck, determine the time during which the spine compartmentalizes calcium.

Action Potentials↗
PubMed1989

Calcium and calcium regulating hormones in the "prehypertensive" Dahl salt sensitive rat (calcium and salt sensitive hypertension).

The purpose of this study was to determine if alterations of calcium and calcium regulating hormones precede the onset of NaCl induced hypertension in the Dahl salt sensitive (S) rat. After a 5 day balance study, serum ionized calcium, PTH, and 1,25 dihydroxy vitamin D concentrations were measured in Dahl-S and salt resistant (R) rats that had been maintained on a "normal" (1%) or high (7%) NaCl intake. Blood pressure was higher in Dahl-S than R (P less than .01), but was not affected by 5 days of high NaCl. On both NaCl intakes, urine calcium excretion was increased, serum calcium was decreased, and serum PTH and 1,25 dihydroxy vitamin D were increased in Dahl-S compared to Dahl-R (P less than .01). On the high NaCl intake, fecal calcium was greater in Dahl-S than in Dahl-R, and net 5 day calcium balance was less positive in Dahl-S (P less than .05). In contrast to NaCl, a high dietary intake of sodium with anions other than chloride (NaAA) fails to produce hypertension in the Dahl-S rat. NaAA loading resulted in decreased urine calcium excretion (P less than .01), and after 5 days of the high NaAA diet, serum calcium and PTH did not differ in Dahl-S and Dahl-R. Thus, alterations of calcium, PTH, and vitamin D precede NaCl-induced hypertension in Dahl-S. These alterations may contribute to the development of hypertension in this animal model.

Animals↗
PubMed1986

Differentiation of calcium entry blockers into calcium channel blockers and calcium overload blockers.

The heterogeneity of the several subgroups of calcium-antagonistic drugs requires a rigid and well-defined differentiation of this type of agents. From the chemical point of view verapamil-like drugs, dihydropyridines, benzothiazepines and diphenylalkylamines should be distinguished. Among these largely different groups no obvious relationship between chemical structure and calcium-antagonistic activity can be recognized. Irrespective of the chemical classification all above-mentioned compounds inhibit the entry of calcium into cells. However, from a pharmacological point of view a distinction should be made between calcium channel blockers and calcium overload blockers. Calcium channel blockers selectively and competitively inhibit the transmembranous slow inward current, which is carried by calcium ions both in cardiac tissues and in vascular smooth muscle under physiological conditions. However, calcium overload blockers only inhibit the overload of the cell with calcium ions, which occurs under pathological, ischemic conditions. Finally, a survey is given of the various subtypes of calcium-antagonistic drugs with respect to their organ specificity and therapeutic applicability.

Animals↗
PubMed1985

Calcium citrate: reduced propensity for the crystallization of calcium oxalate in urine resulting from induced hypercalciuria of calcium supplementation.

The effect of calcium citrate (800 mg calcium/day in 4 divided doses) on urinary biochemistry and crystallization of calcium salts was examined in 18 normal subjects. During treatment, urinary calcium increased significantly (from 150 +/- 65 (SD) to 248 +/- 77 mg/day). Urinary citrate rose from 611 +/- 208 to 730 +/- 225 mg/day, owing largely to the alkali load. The urinary saturation of calcium oxalate rose by only 41% during calcium citrate treatment, due mainly to citrate complexation of calcium (rather than by 62% without such complexation). Moreover, the formation product of calcium oxalate rose during treatment, indicating that the enhanced citrate excretion augmented the inhibitor activity against calcium oxalate crystallization. Thus, calcium citrate may not be attendant with the risk for stone formation usually associated with calcium supplementation.

Adult↗
PubMed1990

Adjusted ionized calcium (at pH 7.4) and actual ionized calcium (at actual pH) in capillary blood compared for clinical evaluation of patients with disorders of calcium metabolism.

We report results for adjusted ionized calcium (at pH 7.4) and actual ionized calcium (at actual pH) in capillary blood from 183 patients with disorders of calcium metabolism (primary hyperparathyroidism, secondary hyperparathyroidism of malabsorption, primary hypoparathyroidism, Paget's disease, acromegaly, hypercalcemia of malignancy, osteoporosis, sarcoidosis, idiopathic hypercalciuria, and familial hypocalciuric hypercalcemia). The correlation and the equation for the linear regression between adjusted ionized calcium (y) and actual ionized calcium (x) were y = 1.011x + 0.005 mmol/L, r = 0.992, Sy,x = 0.021 mmol/L. Results were similar within each diagnostic group. Consistent agreement between adjusted and ionized calcium was observed in 96.7% of patients representing a variety of the most frequently encountered disorders of calcium metabolism. Thus we find adjusted ionized calcium to be as useful as actual ionized calcium for evaluation of patients with such disorders. Adjusted ionized calcium may therefore also be a logical choice for establishing agreement between laboratories for reference intervals in healthy adults.

Acromegaly↗
PubMed1988

Interaction of morphine with intrathecally administered calcium and calcium antagonists: evidence for supraspinal endogenous opioid mediation of intrathecal calcium-induced antinociception in mice.

The interaction between morphine [i.p. and intrathecal (i.t.)] and calcium and its antagonists (i.t. and i.c.v.) was studied in the mouse tail-flick test for antinociception. Calcium (0.66 mumol i.t.) produced antinociception comparable to that of morphine (0.5 microgram i.t.) but had a significantly longer duration. A lower dose of calcium (0.16 mumol i.t.) significantly potentiated morphine (0.2 and 0.5 micrograms i.t.). The antinociceptive effect of i.p. morphine was also potentiated by i.t. calcium, but was antagonized by the i.t. administration of ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid (3.7-7.5 nmol), verapamil (15 micrograms), magnesium (9.4 nmol) and barium (1-2 nmol). In contrast, i.t. calcium and i.p. morphine were significantly potentiated by the i.c.v. administration of verapamil (15 micrograms) and antagonized by i.c.v. calcium (0.33 mumol). The antinociceptive effect of i.t. calcium was antagonized by naloxone administered s.c. (1 mg/kg) or i.c.v. (0.5 microgram), but not i.t. (0.5 and 10 microgram). It is concluded that the antinociceptive effect of i.t. calcium is mediated, at least partly, by a reflex supraspinal release of endogenous opioids, and that the administration of calcium and its antagonists modify the antinociceptive effect of morphine in opposite directions, depending upon whether they are administered by the i.t. or i.c.v. routes. Calcium may serve as a useful adjunct for opioid-induced analgesia via the i.t. route.

Analgesics↗
PubMed1994

Calcium balance and serum ionized calcium fluctuations in on-line haemodiafiltration in relation to ultrafiltration rate and dialysate calcium concentration.

The use of high ultrafiltration rates in haemodiafiltration (HDF) has been suggested for improving the clearance of small and large molecules. This strategy has become economically applicable with the development of safe techniques for on-line production of sterile infusate from dialysate, which enables us to infuse large substitution fluid volumes without further increasing the cost of sessions. The effect of increasing the ultrafiltration rate in HDF on electrolyte balance has not yet been evaluated. The aim of this study was to evaluate the effects of variations of the ultrafiltration rate on calcium kinetics in HDF using three different dialysate calcium concentrations. Since the increase in ultrafiltration rate augments the convective calcium loss, variations of intrasession calcium balance could result from modifications of the ultrafiltration rate. In the present study we found no significant variations in calcium balance and serum ionized calcium (iCa) levels during on-line HDF treatment when increasing the mean ultrafiltration rate from 60 to 100 ml/min in the presence of an adequate and corresponding increase in the infusion rate (from 2.5 to 5 l/h). During the balance studies, pretreatment serum iCa was on the average 1.32 mmol/l and weight loss 3.2 kg. Mean calcium loss during treatment was 2.8 and 3.3 mmol at infusion rates of 2.5 and 5 l/h with 1.63 mmol/l of calcium in both the dialysate and infusate; calcium loss rose to 5.9 and 11.2 mmol at infusion rates of 2.5 l/h and to 5.7 and 14.2 mmol at infusion rates of 5 l/h when the dialysate and infusate calcium was reduced respectively to 1.5 and 1.25 mmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium↗
PubMed1994

Bradykinin (Bk) increases cytosolic calcium in cultured rat myenteric neurons via Bk-2 type receptors coupled to mobilization of extracellular and intracellular sources of calcium: evidence that calcium influx is prostaglandin dependent.

We examined the effect of bradykinin (Bk) on cytosolic calcium ([Ca++]i) in cultured rat ileal myenteric neurons. The receptor subtype(s) and calcium pool(s), e.g., extracellular and/or intracellular calcium that mediate Bk's effect on [Ca++]i in myenteric neurons, have not been reported. Superfusion with Bk (10 nM) increased [Ca++]i by 96 +/- 10 nM over basal levels in approximately 80% of the neurons tested that were not affected by a Bk-1 receptor antagonist but were inhibited 72% by a Bk-2 receptor antagonist. The Bk-generated increase in [Ca++]i was reduced by 45% and 52% of control response in calcium-free buffer and indomethacin, respectively, supporting involvement of extracellular and intracellular pools of calcium and mediation, in part, by a prostaglandin-dependent pathway. Bk increased [Ca2++]i by 54 +/- 6 nM in calcium-free buffer that was indomethacin insensitive, suggesting that Bk stimulation of extracellular calcium influx was mediated by a prostaglandin-dependent pathway. Bk (1 microM) increased tissue prostaglandin E2 (PGE2) production by 62% over basal levels in isolated rat ileal myenteric ganglia. Finally, superfusion with PGE2 (10 microM) increased [Ca++]i by 105 +/- 16 nM over basal levels that were blocked in calcium-free buffer. In summary, our studies suggest that cultured rat ileal myenteric neurons express the Bk-2 receptor subtype that is coupled to mobilization of extracellular and intracellular pools of calcium. Bk stimulates influx of extracellular calcium via a prostaglandin-dependent pathway.

Animals↗
PubMed2003

Activation of calcium release assessed by calcium release-induced inactivation of calcium current in rat cardiac myocytes.

In mammalian cardiac myocytes, calcium released into the dyadic space rapidly inactivates calcium current (ICa). We used this Ca2+ release-dependent inactivation (RDI) of ICa as a local probe of sarcoplasmic reticulum Ca2+ release activation. In whole cell patch-clamped rat ventricular myocytes, Ca2+ entry induced by short prepulses from -50 mV to positive voltages caused suppression of peak ICa during a test pulse. The negative correlation between peak ICa suppression and ICa inactivation during the test pulse indicated that RDI evoked by the prepulse affected only calcium channels in those dyads in which calcium release was activated. Ca2+ ions injected during the prepulse and during the subsequent tail current suppressed peak ICa in the test pulse to a different extent. Quantitative analysis indicated that equal Ca2+ charge was 3.5 times less effective in inducing release when entering during the prepulse than when entering during the tail. Tail Ca2+ charge injected by the first voltage-dependent calcium channel (DHPR) openings was three times less effective than that injected by DHPR reopenings. These findings suggest that calcium release activation can be profoundly influenced by the recent history of L-type Ca2+ channel activity due to potentiation of ryanodine receptors (RyRs) by previous calcium influx. This conclusion was confirmed at the level of single RyRs in planar lipid bilayers: using flash photolysis of the calcium cage NP-EGTA to generate two sequential calcium stimuli, we showed that RyR activation in response to the second stimulus was four times higher than that in response to the first stimulus.

Animals↗
PubMed2000

Calcium-induced calcium release in smooth muscle: loose coupling between the action potential and calcium release.

Calcium-induced calcium release (CICR) has been observed in cardiac myocytes as elementary calcium release events (calcium sparks) associated with the opening of L-type Ca(2+) channels. In heart cells, a tight coupling between the gating of single L-type Ca(2+) channels and ryanodine receptors (RYRs) underlies calcium release. Here we demonstrate that L-type Ca(2+) channels activate RYRs to produce CICR in smooth muscle cells in the form of Ca(2+) sparks and propagated Ca(2+) waves. However, unlike CICR in cardiac muscle, RYR channel opening is not tightly linked to the gating of L-type Ca(2+) channels. L-type Ca(2+) channels can open without triggering Ca(2+) sparks and triggered Ca(2+) sparks are often observed after channel closure. CICR is a function of the net flux of Ca(2+) ions into the cytosol, rather than the single channel amplitude of L-type Ca(2+) channels. Moreover, unlike CICR in striated muscle, calcium release is completely eliminated by cytosolic calcium buffering. Thus, L-type Ca(2+) channels are loosely coupled to RYR through an increase in global [Ca(2+)] due to an increase in the effective distance between L-type Ca(2+) channels and RYR, resulting in an uncoupling of the obligate relationship that exists in striated muscle between the action potential and calcium release.

Action Potentials↗
PubMed1981

Effects of a cation exchange resin on intestinal calcium absorption and urinary calcium in calcium stone formers.

The effect on the urinary excretion of calcium of an oral cation exchange resin without phosphorus was studied in healthy control subjects and patients with recurrent calcium lithiasis under out-patient conditions. An immediate reduction of intestinal calcium absorption and urinary calcium excretion was found in five control subjects and in one patient after ingestion of resin, whereas calcium excretion remained unchanged in all other patients during long-term treatment. In addition, signs of mild transitory hyperparathyroidism together with an increase in intestinal calcium transport were observed during treatment. It is suggested that intraluminal binding of calcium ions to the resin leads to substantial changes in calcium metabolism with the result that urinary calcium excretion returns to pre-treatment values.

Adult↗
PubMed1980

Regulation of calcium fluxes in rat pancreatic islets: calcium extrusion by sodium-calcium countertransport.

The mechanisms by which glucose regulates calcium fluxes in pancreatic endocrine cells were investigated by monitoring the efflux of 45Ca from prelabeled and perifused rat pancreatic islets. In the absence of both extracellular calcium and glucose, partial or total removal of extracellular sodium decreases the efflux of 45Ca from prelabeled islets. Glucose also reduces the efflux of 45Ca from islets perifused in the absence of extracellular calcium. This inhibitory effect of glucose on 45Ca efflux is decreased by half when the extracellular concentration of sodium is lowered to 24 mM. In the absence of extracellular calcium but presence of glucose, partial or even total removal of extracellular sodium fails to decrease the efflux of 45Ca. At normal extracellular calcium concentration (1 mM) partial removal of extracellular sodium dramatically increases 45Ca efflux from pancreatic islets. This increase in 45Ca efflux is partially but not totally suppressed by either 16.7 mM glucose or cobalt. It is totally suppressed by 4.4 mM glucose or by the combination of 16.7 mM glucose and cobalt. At normal extracellular calcium concentration, glucose initially reduces and subsequently increases 45Ca efflux. The initial fall is unaffected by tetrodotoxin but decreased by 50% at low extracellular sodium concentration (24 mM). The present results suggest the existence in pancreatic endocrine cells of a glucose-sensitive process of sodium-calcium counter-transport. By inhibiting such a process, glucose may decrease the efflux of calcium from islet cells. The effect of glucose is not mediated by an increase in intracellular sodium concentration. It could contribute to the intracellular accumulation of calcium which is thought to trigger insulin release.

Animals↗
PubMed1984

Dantrolene does not block calcium pulse-induced calcium release from a putative calcium channel in sarcoplasmic reticulum from malignant hyperthermia and normal pig muscle.

Calcium pulse additions to isolated SR membranes can cause a reversible efflux of calcium. The threshold level of calcium loading at which calcium efflux occurs is lower for SR membranes isolated from malignant hyperthermia susceptible (MHS) swine. Dantrolene, a unique muscle relaxant, had no effect on threshold calcium load, amounts and rates of calcium release from SR isolated from control and MHS skeletal muscle. It is concluded that the putative calcium channel through which this calcium pulse-induced calcium release mechanism occurs is not affected by dantrolene under these experimental conditions.

Animals↗
PubMed1996

A synthetic peptide representing residues 7 to 21 of human luteinizing hormone beta-subunit binds calcium, facilitates calcium uptake by liposomes and possesses sequence similarity to calcium-binding domains of calmodulin.

We have previously demonstrated that a synthetic peptide corresponding to residues 1 to 15 of hFSH-beta-subunit (hFSH-beta-(1-15)) shares sequence homology with the calcium-binding domains of calmodulin (CaM), binds calcium with an affinity similar to that of CaM-binding loop III (CaM III) and facilitates uptake of external calcium by liposomes and cultured rat Sertoli cells. We noted a sequence homologous to hFSH-beta-(1-15) between residues 7 to 21 of the beta-subunits of both hLH and hCG. A peptide amide representing this region of hLH-beta (hLH-beta-(7-21)) and an N-terminal truncated analog (hLH-beta-(10-21)) that more closely resembles the calcium-binding loops of calmodulin were synthesized and tested for their ability to bind 45Ca2+, and facilitate uptake of 45Ca2+ by liposomes. hLH-beta-(7-21) and hLH-beta-(10-21) bound significant amounts of 45Ca2+ with affinities of 1.2 +/- 0.4 and 0.7 +/- 0.3 mM, respectively, values virtually identical to that reported for a synthetic peptide corresponding to CaM III. The two peptides also facilitated specific, concentration-related and saturable uptake of 45Ca2+ by liposomes, which was sensitive to blockade by voltage-independent calcium-channel antagonists. Our data suggest that residues 7 to 21 of the beta-subunit of hLH may be associated with the previously demonstrated calcium requirement for specific binding of LH to its receptor, and that the calcium-binding property of this region is related to its ability to facilitate uptake of calcium into liposomes via the formation of calcium-conducting transmembrane channels.

Animals↗
PubMed1985

Plasma calcium control in the rat fetus. III. Influence of alterations in maternal plasma calcium on fetal plasma calcium level.

Acute maternal alterations in plasma calcium were used as an indirect mean to study the placental transfer of calcium in thyroparathyroidectomized (TPTX) pregnant rats. Calcium infusions to normal or TPTX females showed in both cases a saturation mechanism reflected on fetal plasma calcium. With TPTX mothers saturation curves of the fetal plasma calcium were similar whether fetuses were decapitated (deprived of brain, hypophysis, and thyroparathyroid complex) or intact. Increments in fetal plasma calcium were 4-fold higher in TPTX mothers (approximately 2.5 mg/dl), and 2-fold higher in thyroidectomized (TX) mothers (approximately 0.5 mg/dl). From the whole results, it appeared that increments in fetal plasma calcium secondary to maternal calcium infusion were probably related to the basal plasma calcium in the fetus, and not to the hormonal deficiency of the mother.

Animals↗