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PubMed1989

Four intracisternal calcium-binding glycoproteins from rat liver microsomes with high affinity for calcium. No indication for calsequestrin-like proteins in inositol 1,4,5-trisphosphate-sensitive calcium sequestering rat liver vesicles.

It has been claimed that the inositol 1,4,5-trisphosphate-sensitive calcium pool in liver and pancreatic acinar cells is located in specified organelles ("calciosomes") which are characterized by their content of the calcium-binding protein calsequestrin (Volpe, P., Krause, K. H., Hashimoto, S., Zorzato, F., Pozzan, T., Meldolesi, J., and Lew, D. P. (1988) Proc. Natl. Acad. Sci. U. S. A. 85, 1091-1095). We show here that the inositol 1,4,5-trisphosphate-sensitive compartment of rat liver does not contain calsequestrin-like material. Instead four non-membraneous calcium-binding glycoproteins with approximate molecular masses of 59, 60, 80, and 90 kDa were found. The 59-, 80-, and 90-kDa proteins were of the high mannose-rich type, the carbohydrate moiety of the 60-kDa protein was of the complex hybrid type with terminal galactoses. All four proteins had high affinity binding sites for calcium (KD between 1 and 5 microM) and from 1 to 5 binding sites/molecule. The 80- and the 90-kDa proteins had also low affinity binding sites (KD 400 and 600 microM, respectively, with 13 and 15 binding sites/molecule, respectively). A comparison of the NH2-terminal sequences revealed that the 60-kDa calcium-binding protein represents the rat liver calregulin, whereas the 90-kDa calcium-binding protein represents grp94. The sequences did not reveal any relationship of the 80-kDa protein with grp78, or of the 59-kDa protein with protein disulfide isomerase.

Amino Acid Sequence↗
PubMed1983

[Calcium antagonism - a new pharmacologic principle in resuscitation. Comparison of calcium and calcium antagonists].

In cardiopulmonary resuscitation (CPR) of dogs after anoxic cardiac arrest the effect was compared of epinephrine (E) alone (50 micrograms/kg, n = 11) to that of epinephrine plus calcium chloride (20 mg/kg) and of diltiazem (150 micrograms/kg 30 sec after E and 25-50 micrograms/kg/min after restoration of spontaneous circulation). The success of resuscitation was 100% in the epinephrine group and the diltiazem group but only 70% in the calcium group (p less than 0.05). In the phase of restoration of spontaneous circulation, calcium increased the critical hemodynamic parameters leading to O2 consumption whereas diltiazem decreased them (heart rate, LVdp/dt max, afterload). Diltiazem improved the oxygen demand/supply ratio by increasing coronary blood flow significantly and decreasing oxygen demand. The significant increase in CPK activity reflected unfavorable oxygen balance in the calcium group. It is concluded that calcium should not be given in CPR, although calcium antagonism represents a promising new pharmacological principle in this field.

Animals↗
PubMed1975

Radioimmunoassay studies of intestinal calcium-binding protein in the pig. I. Identification of intestinal calcium-binding protein in blood and response to a low calcium diet.

We have developed a radioimmunoassay for porcine intestinal calcium-binding protein (CaBP) and have used it to detect CaBP in pig plasma. Plasma CaBP is identical to intestinal CaBP on the basis of immunological activity, molecular size, and molecular charge properties. The plasma CaBP concentration was greater in the portal blood than in mixed venous blood, suggesting that blood CaBP originates in the gut. Two of four 15-week-old littermate pigs were placed on a low calcium diet (0.15% calcium, 0.65% phosphorus) and two on a control diet (0.65% calcium, 0.65% phosphorus). After 2 weeks, the entire small intestine was removed and divided into nine 1.8-m segments. CaBP was assayed in both plasma and intestinal mucosa. When the two pigs on a low calcium diet were compared with two control pigs, there was a general increase in immunoreactive CaBP in both plasma and intestinal mucosa. However, there was no increment in immunoreactive CaBP in the first 1.8-m segment of small intestine. Seventy-one percent of the increment in CaBP occurred distal to the first two segments. The largest fractional low calcium diet effect occurred in the ileum. The mean CaBP concentration for the total small intestine increased by a factor of 1.9. The plasma CaBP concentration increased by a factor of 2.6. In these pigs, plasma CaBP was a more reliable indicator of change in CaBP status than was the measurement in the proximal gut segment which contained the duodenum. The assay of CaBP in blood is convenient and may obviate the sampling errors inherent in intestinal biopsy.

Animals↗
PubMed1988

Adrenergic inhibition of the stimulatory effect of 3,5,3'-triiodothyronine on calcium accumulation and cytoplasmic free calcium concentration in rat thymocytes. Further evidence in support of the concept that calcium serves as the first messenger for the prompt action of thyroid hormone.

Thyroid hormone produces a prompt, plasma membrane-mediated increase in several metabolic functions in the rat thymocyte. These effects of thyroid hormone require calcium and are inhibited by the beta-adrenergic antagonist alprenolol. In the present study, the interrelationship between thyroid hormone and adrenergic agents, and the concept that calcium serves as the first messenger for the rapid action of thyroid hormone in the rat thymocyte are further examined. T3 produced a very rapid and dose-related increase in both 45 calcium accumulation and cytoplasmic free calcium concentration. These effects of T3, like its other calcium-dependent and prompt effects, were inhibited by beta-, but not by alpha-, adrenergic antagonists. Studies with selective beta-adrenergic agents revealed that the inhibitory effect was beta-1 in nature. In addition, beta-adrenergic agonists were found to promote additively T3 action, possibly through their beta-2 activity. Hence, the present study provides further support for the concept that calcium serves as the first messenger in the rapid, plasma membrane-mediated action of thyroid hormone in the rat thymocyte.

Adrenergic alpha-Antagonists↗
PubMed1985

1,25-Dihydroxycalciferol and calcium therapy in osteoporosis with calcium malabsorption. Dose response relationship of calcium absorption and indices of bone turnover.

We have studied some effects of small doses of 1,25-dihydroxycalciferol (calcitriol) and calcium, either combined or separately, in 45 patients with osteoporosis and malabsorption of calcium. In 24 patients on 0.25 micrograms/d of calcitriol the hourly fractional rate of radiocalcium absorption rose from 0.37 +/- 0.02 to 0.55 +/- 0.04 (p less than 0.001) and in 21 patients on 0.50 micrograms/d it rose from 0.36 +/- 0.02 to 0.69 +/- 0.05 (p less than 0.001). These responses were seen within 5 days and were not increased further at 6 weeks to 3 months. The combined therapy significantly reduced the fasting urinary hydroxyproline/creatine ratio (OHPr/Cr) and plasma alkaline phosphatase activity (ALP) in 6-12 weeks, the smaller dose of calcitriol (0.25 micrograms/d) being as effective as the larger one (0.50 micrograms/d) in this respect. Calcium alone (1 g/d) had no effect and calcitriol alone (0.25 mcg/d) had a lesser effect on both OHPr/Cr and ALP than the combined therapy. The falls in OHPr/Cr and ALP tended to be greatest in the cases with the highest initial levels but constituted only partial suppression of these variables towards the theoretical non-bone components. These results suggest that treatment with calcitriol and calcium suppresses bone resorption in osteoporosis associated with malabsorption of calcium and is more effective than calcium or calcitriol given alone.

Alkaline Phosphatase↗
PubMed1983

"Calcium antagonists": a class of drugs with a bright future. Part I. Cellular calcium homeostasis and calcium as a coupling messenger.

The aim of this series of minireviews is to present material from multidisciplinary sources to facilitate the understanding of the pharmacology and the ample clinical potential of a class of drugs that were originally designated as "calcium antagonists" and more recently have been referred to as "calcium entry blockers", "calcium slow channel blockers" or "calcium modulators". In this first report our attention will be focussed on the pivotal role of Ca++ as a messenger linking stimuli of extracellular origin to the intracellular environment. Eucaryotic cells have a number of powerful means to control their cytosolic Ca++ concentration. Firstly, in a cell at rest the cellular membrane is relatively impermeable to passive Ca++ movements. This property of the plasmalemma prevents the high free Ca++ concentration (approximately 1 mM) of the extracellular compartment from invading the cytosol (approximately 0.1 microM). However, extracellular Ca++ can reach the cytosol through the Na+/Ca++ exchange mechanism and the plasmalemma possesses special Ca++ channels the conductance of which is controlled by gates that are opened by critical changes in cellular polarization (voltage-operated channels: VOC) or by receptor activation (receptor-operated channel: ROC). The Ca++ entering via VOC or ROC can subsequently trigger the liberation of Ca++ from the sarcoplasmic reticulum or from calcium stores located in the inner side of the plasmalemma. The intracellular message generated by external stimuli is transferred to the response mechanism by several cytosolic proteins that require Ca++ as activator. Finally, the termination of the response is the result of a reduction in the cytosolic Ca++ concentration that is accomplished by the Na+/Ca++ exchange mechanism or by energy-dependent pumps which extrude Ca++ from the cell or store it in subcellular organelles. Therefore, any of the numerous steps of the excitation-response coupling which employ Ca++ as a messenger or as a protein activator can be the site of action of a pharmacological agent. In the follow-up minireview, some methods to determine the basic pharmacological profile of compounds interfering with cellular Ca++-dependent functions will be described.

Action Potentials↗
PubMed2000

How calcium influx through calcium leak channels is responsible for the elevated levels of calcium-dependent proteolysis in dystrophic myotubes.

Duchenne muscular dystrophy patients lack the protein dystrophin which is an essential link in the complex of proteins that connect the cytoskeleton to the extracellular matrix. In mechanically stressed tissues such as muscle, transient sarcolemmal microdisruptions are normal, but in dystrophic muscle cells the frequency of these microdisruptions is greatly increased. Although both normal and dystrophic cells are able to actively repair these microdisruptions, calcium entry through the more frequent sarcolemmal microdisruptions of dystrophic cells results in an increased calcium-dependent proteolysis that alters the activity of the calcium leak channel. The accumulation of abnormally active calcium leak channels over time results in a gradual loss of calcium homeostasis and eventual cell death.

Animals↗
PubMed2001

Nerve evoked P2X receptor contractions of rat mesenteric arteries; dependence on vessel size and lack of role of L-type calcium channels and calcium induced calcium release.

1. Contractile responses to short trains of nerve stimulation have been characterized in small, medium and large arteries from the rat mesenteric circulation (5th - 6th, 2nd - 3rd and 1st order, respectively). In addition, sources of calcium for smooth muscle contraction have been investigated. 2. Nerve stimulation (10 pulses at 10 Hz) evoked reproducible contractions. The P2 receptor antagonist suramin (100 microM) reduced constrictions by 65.3+/-7.4, 82.7+/-3.3 and 3.1+/-6.1% in small, medium and large arteries respectively. The alpha-adrenoceptor antagonist prazosin (0.1 microM) reduced responses by 32.6+/-2.6, 27.0+/-1.5 and 97.0+/-1.9% respectively. 3. The L-type calcium channel antagonist nifedipine (1 microM) reduced nerve-evoked contractions by 2.8+/-3.3, 10.0+/-3.7 and 13.5+/-2.7% in small, medium and large arteries respectively. When the adrenergic component of contraction was blocked by prazosin (0.1 microM) nifedipine reduced responses by 4.6+/-7.9, 14.3+/-2.0 and 3.0+/-1.9% respectively. Contractile responses to exogenous alpha,beta-meATP were unaffected by the depletion of calcium stores with cyclopiazonic acid (30 microM). This indicates that mobilization of calcium from internal stores is not required for P2X receptor mediated smooth muscle contraction. We conclude that for neurogenic responses, the P2X receptor mediated component of constriction dominates in small mesenteric arteries (3rd -- 6th order) while in large arteries (1st order) noradrenaline mediates contraction. For P2X receptor mediated responses all the calcium required for smooth muscle contraction enters the cell directly through P2X receptor channels.

Animals↗
PubMed1988

Heterogeneity of lymphocyte calcium metabolism is caused by T cell-specific calcium-sensitive potassium channel and sensitivity of the calcium ATPase pump to membrane potential.

Calcium management differs in T and B lymphocytes. [Ca2+]i elevation in response to calcium ionophores is up to 10 times greater in T cells than B cells. There is no difference between them in ionophore uptake. T cells, but not B cells, possess a calcium-sensitive potassium channel which produces membrane hyperpolarization at [Ca2+]i above 200 nM. This alters T cell density providing a rapid and easy method of cell separation. In contrast, B cells depolarize when [Ca2+]i is increased. Isolated B cell membrane vesicle ATP-dependent calcium pump activity is higher than T cell vesicles. Membrane depolarization reduces the [Ca2+]i response to ionomycin, most dramatically in T cells because they are hyperpolarized by increased [Ca2+]i. The most likely basis of this behavior is an effect of membrane potential on lymphocyte membrane calcium pump activity. This mechanism provides an explanation of the inhibitory effect of membrane depolarization on T lymphocyte responses.

Animals↗
PubMed1999

Is there a role for uric acid in an animal model of calcium phosphate nephrocalcinosis and calcium phosphate crystallization in urine of patients with idiopathic calcium urolithiasis? An orientational study.

Uric acid (UA), a waste product of purine metabolism, may be involved in calcium phosphate crystallization and deposition. Rats, which develop nephrocalcinosis on high-fat or magnesium-deficient diets, and patients with idiopathic calcium urolithiasis have hyperproteinuria, especially of nonalbumin protein, and a shift toward elevated serum UA. In rats, an increase in UA precursors and renal UA suggests hypoxemia, which stimulates xanthine oxidase. In patients, a primary increase in renal xanthine oxidase would explain the low urine UA in the presence of an elevated serum concentration. For calcium phosphate deposition (rats) or incorporation into stones (humans) to occur, a crucial factor may be xanthine oxidase-mediated overproduction of free radical species and subsequent tissue damage. Another factor may be whether sufficient UA is synthesized to neutralize these free radicals. Allopurinol use, which inhibits xanthine oxidase and has long been favored for the treatment of idiopathic calcium urolithiasis, may not prevent stones, because it also diminishes the availability of UA. An investigation of the factors that control serum UA homeostasis may be rewarding in research into the etiology of idiopathic calcium urolithiasis.

Animals↗
PubMed1999

Effects of calcium channel blockers on calcium release-activated calcium currents in rat hepatocytes.

AIM: To study the influences of calcium channel blockers on calcium release-activated calcium currents (ICRAC) in rat hepatocytes. METHODS: Whole-cell patch-clamp technique was used. RESULTS: The peak amplitude of ICRAC was -0.41 nA +/- 0.09 nA (n = 15), its reversal potential was about 0 mV. Verapamil (Ver), diltiazem (Dil), and nifedipine (Nif) decreased ICRAC strikingly, without affecting its reversal potential. The inhibitory rate of Ver 5 mumol.L-1 was 40% +/- 12% (n = 3), Ver 50 mumol.L-1 reduced the peak amplitude of ICRAC from -0.49 nA +/- 0.12 nA to -0.20 nA +/- 0.09 nA (P < 0.01 vs control, n = 5). The inhibitory rate was 57% +/- 15%. Dil 50 mumol.L-1 and Nif reduced ICRAC from -0.43 nA +/- 0.10 nA to -0.29 nA +/- 0.07 nA (P < 0.01 vs control, n = 5), from -0.32 nA +/- 0.08 nA to -0.27 nA +/- 0.08 nA (P < 0.01 vs control, n = 5). The inhibitory rate was 31% +/- 11%, 19% +/- 7%, respectively. The amplitude of ICRAC was dependent on extracellular Ca2+ concentration. The peak amplitude of ICRAC was -0.21 nA +/- 0.08 nA (n = 3) in Tyrode's solution with Ca2+ 1.8 mmol.L-1 (P < 0.01 vs the peak amplitude of ICRAC in external solution with Ca2+ 10 mmol.L-1). CONCLUSION: The three calcium antagonists inhibited ICRAC effectively and protected hepatocytes from calcium overload via the inhibition of ICRAC.

Animals↗
PubMed2004

Biophysical and pharmacological characterization of spermatogenic T-type calcium current in mice lacking the CaV3.1 (alpha1G) calcium channel: CaV3.2 (alpha1H) is the main functional calcium channel in wild-type spermatogenic cells.

Mammalian acrosome reaction (AR) requires successive activation of three different types of calcium channels (T-type channels, Inositol-3-phosphate (InsP3) receptors, and TRPC2 channels). All the calcium signaling is under the control of the activation of the first-one, a T-type calcium channel. The molecular characterization of the T-type calcium channel is still a matter of debate, previous reports showing the presence of transcripts for Ca(V)3.1 and Ca(V)3.2 subunits. Using mice deficient for Ca(V)3.1 subunit, we show that the T-type current density in spermatogenic cells is not reduced in deficient mice versus control mice. We characterized the biophysical and pharmacological properties of T-type current in spermatogenic cells from Ca(V)3.1 deficient mice. Biophysical and pharmacological properties of spermatogenic T-type current from wild-type and Ca(V)3.1 deficient mice demonstrate that Ca(V)3.3 does not contribute to T-type current. Moreover, nickel and amiloride inhibit T-type currents in deficient and wild-type mice with similar potencies. These results demonstrate that T-type currents in spermatogenic cells is due to Ca(V)3.2 subunit and that Ca(V)3.1 contributes to a very negligible extent to the T-type currents. Thus, the deficient Ca(V)3.1 mouse model allows the characterization of native Ca(V)3.2 currents in spermatogenic cells. Spermatogenic Ca(V)3.2 currents present specific feature in comparison to the cloned Ca(V)3.2 current so far. More particularly, the time-dependence of recovery from short-term inactivation of native spermatogenic Ca(V)3.2 is close to 100 millisecond, a value expected for Ca(V)3.1 current.

Amiloride↗
PubMed1976

The subcellular localization of calcium in vertebrate smooth muscle; calcium-containing and calcium-accumulating structures in muscle cells of mouse intestine.

The intracellular localization of calcium by means of cytochemical techniques was studied in smooth muscle cells of mouse intestine. When the lead acetate method according to Carasso and Favard (1966) was used calcium was found in mitochondria and sarcoplasmic reticulum and occasionally between the myofilaments. The active ATP-dependent accumulation of calcium into cell structures was investigated by the oxalate method (Heumann and Zebe, 1967). After appropriate treatment the only structures of smooth muscle cells which contained calcium oxalate (identified by microprobe analysis) were elements of the sarcoplasmic reticulum. The results are discussed in relation to the role of calcium in the control of muscle activity during the contraction-relaxation cycle.

Acetates↗
PubMed1993

Calcium wave propagation by calcium-induced calcium release: an unusual excitable system.

We discuss in detail the behaviour of a model, proposed by Goldbeter et al. (1990. Proc. natn. Acad. Sci. 87, 1461-1465), for intracellular calcium wave propagation by calcium-induced calcium release, focusing our attention on excitability and the propagation of waves in one spatial dimension. The model with no diffusion behaves like a generic excitable system, and threshold behaviour, excitability and oscillations can be understood within this general framework. However, when diffusion is included, the model no longer behaves like a generic excitable system; the fast and slow variables are not distinct and previous results on excitable systems do not necessarily apply. We consider a piecewise linear simplification of the model, and construct travelling pulse and periodic plane wave solutions to the simplified model. The analogous behaviour in the full model is studied numerically. Goldbeter's model for calcium-induced calcium release is an excitable system of a type not previously studied in detail.

Animals↗
PubMed1995

Calcium-dependent conformation of a mouse macrophage calcium-type lectin. Carbohydrate binding activity is stabilized by an antibody specific for a calcium-dependent epitope.

We established monoclonal antibodies (mAbs) against the mouse macrophage galactose/N-acetylgalactosamine-specific lectin (MMGL) that is a 42-kDa calcium-dependent lectin, using a solid phase carbohydrate binding assay as a novel strategy for screening mAbs. The specificity of six mAbs were investigated by antibody binding to native or recombinant forms (rML) of MMGL, flow cytometry, and immunoprecipitation using a macrophage cell line RAW264.7. Four of these mAbs strongly inhibited the binding of fluorescein 5-isothiocyanate-labeled galactosylated polylysine to immobilized rML, one inhibited moderately, and one did not inhibit binding. The competitive binding study revealed that the binding sites of these four blocking mAbs were closely related to each other but were different from the rest of these mAbs. A non-blocking mAb having a unique binding specificity (LOM-11) exhibited calcium-dependent binding to rML, suggesting that calcium-dependent epitope was not situated in the vicinity of the ligand binding site. Furthermore, pretreatment of rML with the mAb LOM-11 preserved ligand binding activity, especially in a low calcium environment. The four blocking mAbs mentioned above facilitated the binding of the mAb LOM-11 to rML. These results indicate that there is a positive cooperativity between the lectin's ligand binding site and its physically distinct calcium-dependent epitope.

Animals↗
PubMed1990

Prostaglandin F2 alpha-induced calcium transient in ovine large luteal cells: I. Alterations in cytosolic-free calcium levels and calcium flux.

The effect of prostaglandin F2 alpha (PGF2 alpha) on cytosolic calcium homeostasis was studied in suspensions of ovine large or small luteal cells from superovulated ewes. In large cells loaded with fura-2 (AM), resting cytosolic-free calcium ([Ca2+]i) was 62 +/- 5 nM (Hanks' medium, pH 7.15), and PGF2 alpha (0.5 microM) induced a rapid transient increase in [Ca2+]i to 152 +/- 6 nM, which then decreased to 97 +/- 6 nM within 3 min and remained at this level for the remainder of the treatment period (10-20 min). PGF2 alpha did not alter intracellular pH (pHi) in cells loaded with snarf-1 (AM) (pHi indicator). The transient nature of the [Ca2+]i increase was due, at least in part, to the ability of PGF2 alpha to stimulate (P less than 0.05) 45Ca2+ efflux. In small cells, resting [Ca2+]i was 57 +/- 5 nM, and no change in [Ca2+]i levels or pHi occurred with the addition of PGF2 alpha. PGF2 alpha also did not affect 45Ca2+ efflux in small cells. Calcium uptake was not significantly altered by PGF2 alpha in large or small cells. Data from kinetic analysis of the calcium transient was best fit to a two-compartment model consisting of a rapidly effluxing compartment and a slowly effluxing compartment. The size and rate constants were 62 +/- 10 nM and 3.6 +/- 1 min-1, respectively, for the rapidly effluxing compartment and 140 +/- 9 nM and 0.02 +/- 0.002 min-1, respectively, for the slowly effluxing compartment. These results provide evidence for a direct effect of PGF2 alpha specifically on the ovine large luteal cell that involves alterations in [Ca2+]i and calcium flux. This effect is likely to be involved in intracellular mediation of the signal for luteal regression.

Animals↗
PubMed1991

Short-term effects of low-calcium dialysis solutions on calcium mass transfer, ionized calcium, and parathyroid hormone in CAPD patients.

Patients on CAPD using calcium carbonate (CaCO3) as phosphate binder might benefit from low-calcium (Ca) concentration dialysis solutions; however, no data are available for the effects of this regimen on Ca metabolism. We studied 10 patients on stable CAPD regimens with standard dialysis solutions (Ca 7 mg/dL) who were taking CaCO3 to control hyperphosphatemia (mean daily doses 4.5 +/- 2.4 g). Hypercalcemic episodes had been recorded in 6 patients. Standard dialysis solutions were replaced with solutions containing 5 mg/dL of Ca. Calcium and phosphate peritoneal mass transfer (MT), serum concentrations of total Ca, ionized Ca (Ca++), phosphate, intact PTH, and mid-molecular PTH, were evaluated before and 48 hours after change of dialysate. The switch to low-Ca solutions was accompanied by significant changes in calcium mass transfer (Ca MT) (+9.84 +/- 48.22 versus -96.74 +/- 48.32 mg/day, p less than .001). Ca MT was significantly (p less than .05) correlated with the serum/dialysate Ca gradient. There was no difference in phosphate MT. Serum Ca++ significantly (p less than .05) decreased from 5.20 +/- 0.32 to 4.88 +/- 0.36 mg/dL, and intact PTH significantly increased (81.5 +/- 139 versus 112.4 +/- 168 pg/mL, p less than .05). It is concluded that dialysis solutions with Ca 5 mg/dL result in a negative peritoneal Ca MT and can be useful to prevent and treat hypercalcemia in CAPD patients taking CaCO3 as phosphate binder. A careful monitoring of ionized calcium, PTH, and phosphate is suggested when an extensive and long-term use of this solution is considered.

Adult↗