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PubMed1990

Action of antiepileptic and anaesthetic drugs on Na- and Ca-spikes in mammalian non-myelinated axons.

The actions of the antiepileptic drugs phenytoin, carbamazepine and phenobarbitone, and the local anaesthetic drugs lignocaine and procaine on sodium-dependent and calcium-dependent compound action potentials (Na- and Ca-spikes) have been compared in rat preganglionic cervical sympathetic nerves, using extracellular recording techniques. There was no discernible difference in the frequency dependence of Na-spike block over the frequency range 0.2-20 Hz between these two groups of drugs. However the antiepileptic drugs were more potent blockers of the Ca-spike, whereas the local anaesthetics were more potent on the Na-spike. It is proposed that a dual action of antiepileptics, a frequency-dependent block of sodium currents combined with a block of calcium currents, may explain their efficacy in the treatment of seizures.

Action Potentials↗
PubMed2006

Sphingosylphosphorylcholine enhances calcium entry in thyroid FRO cells by a mechanism dependent on protein kinase C.

Several sphingolipid derivatives, including sphingosylphosphorylcholine (SPC), regulate a multitude of biological processes. In the present study we show that both human thyroid cancer cells (FRO cells) and normal human thyroid cells express G protein-coupled receptor 4 (GPR4) and ovarian cancer G protein-coupled receptor 1 (OGR1), putative SPC-specific receptors. In FRO cells SPC evoked a concentration-dependent increase in intracellular free calcium concentration ([Ca2+]i) in a calcium containing, but not in a calcium-free buffer. Sphingosine 1-phosphate (S1P) evoked an increase in [Ca2+]i in both a calcium containing and a calcium-free buffer. The phospholipase C (PLC) inhibitor U 73122 potently attenuated the effect of SPC, suggesting that effects of SPC were mediated by a G protein coupled receptor. Overnight pretreatment of the cells with pertussis toxin did not affect the SPC-evoked response. Interestingly, SPC did not evoke an increase in inositol phosphates, although S1P did so. Furthermore, in cells pretreated with thapsigargin to deplete intracellular calcium stores, SPC still evoked an increase in [Ca2+]i, suggesting that SPC mainly evoked entry of extracellular calcium. When the cells were pretreated with the protein kinase C (PKC) inhibitor GF 109203X, or when the cells were pretreated with PMA for 24 h, the SPC-evoked calcium entry was attenuated. Thus, the SPC-evoked calcium entry was apparently dependent on PKC. In sharp contrast, the increase in [Ca2+]i evoked by S1P was not sensitive to GF 109203X. Furthermore, the calcium entry evoked by the diacylglycerol analog 1-oleoyl-2-acetyl-sn-glycerol was not inhibited by GF 109203X. In addition, SPC decreased the incorporation of 3H-thymidine in a concentration-dependent manner in FRO cells. Taken together, SPC may be an important factor regulating thyroid cancer cell function.

Boron Compounds↗
PubMed1997

Hypotensive effects of YM430, a 1,4-dihydropyridine derivative, in spontaneously hypertensive rats and renal hypertensive dogs.

The hypotensive effects of YM430 (4(((S)-2-hydroxy-3-phenoxypropyl)amino)butyl methyl 2,6-dimethyl-((S)-4-(m-nitrophenyl))-1,4-dihydropyridine-3,5-dicarboxyla te) were evaluated in hypertensive animals. In conscious spontaneously hypertensive rats (SHR), single oral administration of YM430 (10-100 mg/kg) produced a dose-dependent decrease in mean blood pressure (MBP) with slight reflex tachycardia. The hypotensive effect of YM430 reached its maximum about 2 hr after dosing and lasted for over 10 hr. Importantly, the beta 1-adrenoceptor blocking activity of YM430 had a similar time course to that of its calcium entry blocking activity. In conscious normotensive dogs (NTD: 1-10 mg/kg, p.o.), YM430 decreased MBP without reflex tachycardia, and inhibited isoproterenol (ISO)-induced tachycardia in a dose-dependent manner. In conscious renal hypertensive dogs (RHD: 0.3-3 mg/kg, p.o.), YM430 also produced a sustained hypotensive effect. Furthermore, on repeated oral administration to conscious SHR and NTD, YM430 caused a long-lasting hypotensive effect. This hypotensive activity and inhibition of ISO-induced tachycardia showed neither tolerance, augmentation nor rebound. In conclusion, YM430 has a long-lasting hypotensive effect and behaves as a hybrid compound, combining calcium entry blocking and beta 1-adrenoceptor blocking activities in vivo. In addition, the degree of the blocking activities of YM430 remains nearly constant in the long-term after oral administration.

Administration, Oral↗
PubMed2003

Thrombin downregulates muscle acetylcholine receptors via an IP3 signaling pathway by activating its G-protein-coupled protease-activated receptor-1.

Regulation of thrombin activity may be required during skeletal muscle differentiation since the thrombin tissue inhibitor protease nexin-1 appears at the myotube stage before being localized at the neuromuscular synapse. Here, we have used a model of rat fetal myotube primary cultures to study the effect of thrombin on acetylcholine receptor (AChR) expression, which is enhanced at the myotube stage. Our results show that thrombin decreases both the number of surface AChRs (AChRn) and AChR alpha-subunit gene expression. Using the agonist peptide SFLLRN, we establish that the AChRn decrease is mediated by the G protein-coupled thrombin receptor "protease-activated receptor-1" (PAR-1). Moreover, the specific thrombin inhibitor hirudin increases AChRn by inhibiting the thrombin intrinsically present in the cultures. We further demonstrate that the activation of PAR-1 by thrombin induces intracellular calcium movements that are blocked by 2-APB, an inhibitor of inositol 1,4,5-triphosphate (IP3)-induced calcium release. These calcium signals are more intense in nuclei than in the cytoplasm and are consistent with the intracellular distribution of IP3 receptor that we find in the cytoplasm in a cross-striated pattern and at a high level in the nuclear envelope zone. Finally, we show that the blockade of these IP3-induced calcium signals by 2-APB prevents the AChRn decrease induced by thrombin. Our results thus demonstrate that thrombin downregulates AChR expression by activating PAR-1 and that this effect is mediated via an IP3 signaling pathway.

Acetylcholine↗
PubMed1988

Mammalian cell transformation induced by chromium(VI) compounds in the presence of nitrilotriacetic acid.

We used a soft agar assay on cultured Syrian hamster fibroblasts to determine the ability of nitrilotriacetic acid (NTA) and Cr(VI) compounds to induce malignant cell transformation. Induction of extended anchorage-independent growth was detected in BHK 21/c13 cells by scoring colonies of transformed cells visible to the naked eye 20-25 d after plating in growth medium containing agar. Survival was determined by plating cells in liquid medium without agar and by counting the number of macroscopic colonies after 7-10 d. Mitomycin C and 4-nitroquinoline 1-oxide were used as reference direct transforming agents, with clearly positive results. In our hands no increase of the spontaneous transformation rate of BHK cells was induced by NTA concentrations ranging from 2 X 10(-3) to 10(-2) M, although the survival index was significantly reduced above 4 X 10(-3) M NTA. Two Cr(VI) compounds, K2Cr2O7, which is highly soluble in water, and CaCrO4, which is partially soluble, were tested in the soft agar assay either in the absence or in the presence of NTA. When used alone, both compounds behaved as positive transforming agents. NTA increased 4 or 10 times the cytotoxicity and the transforming activity of CaCrO4 and K2Cr2O7, respectively. As the amounts of soluble Cr(VI) detectable in the K2Cr2O7 and CaCrO4 solutions were not increased in the presence of NTA, a synergistic interaction between NTA and soluble Cr(VI) is inferred.

Acetates↗
PubMed2006

Role of store-operated calcium channels and calcium sensitization in normoxic contraction of the ductus arteriosus.

BACKGROUND: At birth, the increase in oxygen causes contraction of the ductus arteriosus, thus diverting blood flow to the lungs. Although this contraction is modulated by substances such as endothelin and dilator prostaglandins, normoxic contraction is an intrinsic property of ductus smooth muscle. Normoxic inhibition of potassium channels causes membrane depolarization and calcium entry through L-type calcium channels. However, the studies reported here show that after inhibition of this pathway there is still substantial normoxic contraction, indicating the involvement of additional mechanisms. METHODS AND RESULTS: Using ductus ring experiments, calcium imaging, reverse-transcription polymerase chain reaction, Western blot, and cellular electrophysiology, we find that this depolarization-independent contraction is caused by release of calcium from the IP3-sensitive store in the sarcoplasmic reticulum, by subsequent calcium entry through store-operated channels, and by increased calcium sensitization of actin-myosin filaments, involving Rho-kinase. CONCLUSIONS: Much of the normoxic contraction of the ductus arteriosus at birth is related to calcium entry through store-operated channels, encoded by the transient receptor potential superfamily of genes, and to increased calcium sensitization. A clearer understanding of the mechanisms involved in normoxic contraction of the ductus will permit the development of better therapy to close the patent ductus arteriosus, which constitutes approximately 10% of all congenital heart disease and is especially common in premature infants.

Animals↗
PubMed1982

Calcium causes the biphasic dose-response curve for pancreatic amylase secretion.

High concentrations of bethanechol (10(-4) to 10(-3) M) were effective stimulants of amylase secretion from the mouse pancreas if incubations are performed in low [Ca2+] (0.1 mM) solutions but not if normal Krebs solution (2.56 mM Ca2+) was used. This inhibitory effect of Ca2+ at high secretagogue concentrations did not appear to be mediated through the microtubules or microfilaments.

Amylases↗
PubMed2001

Evaluation of the use of Sr2+ in alginate immobilization of cells.

In recent years the method of immobilization of living cells in Ca-alginate beads has gained a wide range of applications. In all cases high chemical stability of the immobilization material and mild conditions for the cells are prerequisites. However, in long-term experiments that may last for several days Ca-alginate may dissolve due to an exchange of Ca2+ with Na+, forming fluid Na-alginate. As well as Ca-alginate, the more chemically stable Sr-alginate and Ba-alginate are materials that have been used for the immobilization of living cells. In this study, the effects of Ca2+, Sr2+ and Ba2+ on growth, viability and intracellular free calcium concentration in a human leukemic T cell line (Jurkat) were investigated. The findings in this study, and the fact that Sr-alginate has a considerably higher chemical stability than Ca-alginate, led to the conclusion that Sr-alginate is a more suitable material for use in the entrapment of living cells in long-term studies.

Alginates↗
PubMed1976

[Mechanism of catecholamine release from the sympathetic nerve endings, particularly in its relation tovacetylcholine an experiment on the isolated vas deferens of rats].

UNLABELLED: The mechanism of catecholamine (CA) release induced by transmural stimulation (TS) and the participation of acetylcholine (ACh) in this mechanism were studied using isotonic contraction of excised vas defernse of rats. Furthermore, the inhibitory effect of bretylium (Br) on sympathetic activity was observed. RESULTS: 1) The effects of various kinds of drugs on isotonic contractions induced by TS, exogenous ACh and exogenous noradrenaline (NA) were observed with the results shown in Table 1. The following has been concluded: (1) TS-induced contraction is due to stimulation of the endings of hypogastric nerve (sympathetic nerve), resulting in CA release from adrenergic fiber (AF) and ACh release from cholinergic fiber (CF) in this nerve. (2) The participation of ACh is not indispensable in the CA release from AF induced by TS. (3) Endogenous ACh release from CF by TS brings about CA release under eserine application. (4) CA release by exogenous ACh is not inhibited by ganglion blockade, but is inhibited by atropine, indicating the muscarinic receptor to be in AF endings. 2) Br exerted preferentially the irreversible inhibition on CA release from AF rather than that on ACh release from CF, while it caused a mild reversible inhibition on CA release by exogenous ACh. 3) On the TS contraction that had been abolished irreversibly by Br, NA incubation showed a mild lasting recovery, while methamphetamine (MAP) or calcium (Ca) incubation showed a strong lasting recovery. Furthermore, in this recovery of TS contraction, the incubation with NA or MAP exerted only the recovery of CA release while the Ca incubation exerted the recovery of both CA release and ACH release. It would appear that Br blocks both AF and CF by inhibiting the transmitter-releasing action of Ca.

Acetylcholine↗
PubMed2000

Requirement of the inositol trisphosphate receptor for activation of store-operated Ca2+ channels.

The coupling mechanism between endoplasmic reticulum (ER) calcium ion (Ca2+) stores and plasma membrane (PM) store-operated channels (SOCs) is crucial to Ca2+ signaling but has eluded detection. SOCs may be functionally related to the TRP family of receptor-operated channels. Direct comparison of endogenous SOCs with stably expressed TRP3 channels in human embryonic kidney (HEK293) cells revealed that TRP3 channels differ in being store independent. However, condensed cortical F-actin prevented activation of both SOC and TRP3 channels, which suggests that ER-PM interactions underlie coupling of both channels. A cell-permeant inhibitor of inositol trisphosphate receptor (InsP3R) function, 2-aminoethoxydiphenyl borate, prevented both receptor-induced TRP3 activation and store-induced SOC activation. It is concluded that InsP3Rs mediate both SOC and TRP channel opening and that the InsP3R is essential for maintaining coupling between store emptying and physiological activation of SOCs.

Actins↗
PubMed2004

Uptake of the carborane derivative of cholesteryl ester by glioma cancer cells is mediated through LDL receptors.

PURPOSE: This study was to elucidate the mechanism of cellular uptake of cholesteryl 1,12-dicarba-closo-dodecaboranel-carboxylate (BCH), a new anti-cancer carborane derivative of cholesteryl ester, by glioma cancer cells. METHODS: BCH (solubilized with liposomal formulation) was incubated with SF-763 and SF-767 glioma cell lines in the presence of different amounts of monoclonal anti-LDL receptor antibody for cellular uptake studies. Various amounts of lipoprotein deficient serum (LPDS) were also used during the uptake. The effect of calcium ion and low temperature on BCH uptake were investigated. In addition, the transfer of BCH from liposomes to low-density lipoprotein (LDL) particles was determined through gradient ultracentrifugation. RESULTS: BCH uptake by these glioma cells was significantly inhibited by the monoclonal antibody. The uptake by both cell lines was reversely correlated with the amount of LPDS. The presence of calcium ion promoted the BCH uptake, whereas the low temperature decreased the BCH uptake. After 16 h incubation, about 46% of BCH was transferred from liposomes to LDL particles. CONCLUSIONS: These results strongly suggested that the cellular uptake of BCH (in liposomal formulation) by SF-763 and SF-767 glioma cell lines is mediated through LDL receptors.

Antibodies, Monoclonal↗
PubMed2005

Multiple calcium channels and kinases mediate alpha7 nicotinic receptor neuroprotection in PC12 cells.

alpha7 Nicotinic receptors are calcium permeant and provide neuroprotection against many insults. We investigated the roles of intracellular calcium ions and downstream calcium channels in this protection. The alpha7 agonist GTS-21 prevented pheochromocytoma cell death induced by nerve growth factor + serum deprivation over a 3-day interval. This effect was blocked by the intracellular calcium chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid in a manner that did not appear to involve changes in receptor density. 1,2-Bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid blocked GTS-21-induced protein kinase C activation, a necessary process for protection. The insositol triphosphate calcium-channel blocker xestospongin C and the phospholipases C inhibitor U-73122 blocked protection, ryanodine partially attenuated protection, but the L-type channel antagonist nifedipine had no effect. ERK1/2 but not JNK and p38 were activated by GTS-21, and the ERK phosphorylation inhibitors PD98059 and U0126 blocked protection.

Animals↗
PubMed2002

[A megatrial of ARB in Japan--CASE-J].

Guidelines for antihypertensive therapy by World Health Organization/International Society of Hypertension(WHO/ISH) and the Joint National Committee(JNC) have been widely accepted by doctors in the world. In Japan, those for Japanese patients(JSH2000) were prepared last year by Japanese Society of Hypertension considering the difference in the drug metabolism, life style, frequencies of complications, etc. in the elderly. Although angiotensin II receptor antagonists are recommended as one of the first line treatment in JSH2000, no large-scale studies have been conducted in Japan. Therefore, CASE-J study has been designed in order to examine the efficacy of Candesartan Cilexetil, an angiotensin II receptor antagonist, comparing with that of amlodipine besilate, a calcium antagonist, in high-risk hypertensive patients using the incidence of cardiovascular events as an endpoint. The study was started in September 2001 and 4,000 patients will be recruited by December 2002. The results are expected to be presented at the meeting of International Hypertensive Society held in Fukuoka in 2006.

Adult↗
PubMed2003

Effect of CuO on the efficiency of sulfur capture of Ca-based compounds during coal combustion.

The efficiency of sulfur capture of CaO, Ca(OH)2 and CaCO3 as well as the effect of CuO on them were studied. Results showed that the efficiency of sulfur capture of Ca(OH)2 is the highest among these three compounds. When CuO was used with each of CaO, Ca(OH)2 and CaCO3 at the same time, the efficiency of all of them would rise, and that of Ca(OH)2 raise most. The efficiency of sulfur capture of Ca(OH)2 with CuO is 14.4% higher than that without CuO.

Adsorption↗
PubMed1980

Stoichiometry and apparent dissociation constant of the calcium-arsenazo III reaction under physiological conditions.

In vitro and in situ tests have been run to characterize the reaction of the mettalochromic indicator, arsenazo III, with calcium. Job plots as well as plots of indicator absorbance vs. [Ca2+] at different indicator concentrations show a 1:1 reaction stoichiometry. Equilibrium analysis and analysis using Adair's equation are also consistent with 1:1 complexes being formed and give estimates of 34 and 45 muM for the apparent dissociation constant. In situ tests were carried out using giant neurons from Archidoris monteryensis, a marine gastropod mollusc. Dye absorbance changes were measured during voltage clamp pulses which produced a fixed calcium influx. The dependence of absorbance change on total dye concentration is consistent with the formation of a 1:1 complex of Ca with ArIII if measurements are made during the initial period of the loading pulse, less than 300 ms, although the apparent dependency changes with longer delay in measurements from the onset of the pulse.

Animals↗
PubMed2003

Correlation between spontaneous electrical, calcium and mechanical activity in detrusor smooth muscle of the guinea-pig bladder.

1. To investigate the cellular mechanisms underlying spontaneous excitation of smooth muscle of the guinea-pig urinary bladder, isometric tension was measured in muscle bundles while recording the membrane potential from a cell in the bundle with a microeletrode. Changes in the intracellular calcium concentration ([Ca(2+)](i); calcium transients) were recorded in strips loaded with the fluorescent dye, fura-PE3. 2. In 40% of preparations, individual action potentials and contractions, which were abolished by nifedipine (1 microm), were generated. In the remaining preparations, bursting action potentials and contractions were generated. Contractions were again abolished by nifedipine (1 microm), while higher concentrations of nifedipine (10-30 microm) were required to prevent the electrical activity. 3. Carbachol (0.1 microm) increased the frequency of action potentials and corresponding contractions. Apamin (0.1 microm) potentiated bursting activity and enhanced phasic contraction. Charybdotoxin (CTX, 50 nm) induced prolonged action potentials that generated enlarged contractions. In contrast, levcromakalim (0.1 microm) reduced the frequency of action potentials, action potential bursts and the size of the contractions. 4. Forskolin (0.1 microm), 8-bromoguanosin 3', 5' cyclic monophosphate (8Br-cGMP, 0.1 mm) and Y-26763 (10 microm) suppressed contractions without reducing the amplitude of either action potentials or Ca transients. 5. This paper confirms that action potentials and associated calcium transients are fundamental mechanisms in generating spontaneous contractions in smooth muscles of the guinea-pig bladder. However, in parallel with the excitation-contraction coupling, the sensitivity of the contractile proteins for Ca(2+) may play an important role in regulating spontaneous excitation and can be modulated by cyclic nucleotides and Rho kinase.

Action Potentials↗
PubMedDate not supplied

An assessment of the tumorigenic properties of a Hudson County soil sample heavily contaminated with hexavalent chromium.

During much of this century, Hudson County, New Jersey, was a major center for the processing of chromium ore. Some of the residue from this processing was used in landfills and in construction materials throughout the county and, in some cases, in highly populated areas. Given that it is widely accepted that exposure to hexavalent chromium compounds poses a risk for the development of respiratory-tract cancer, concerns were raised that individuals who worked or resided in chromium-contaminated areas might be at increased risk for the development of respiratory cancer. To address these concerns, we evaluated a Hudson County soil sample-heavily contaminated with chromium ore residue (Cr(+6) concentration at 5 895 mg/kg)-with respect to its carcinogenic potential to the respiratory tract of Sprague-Dawley rats. Groups of animals were given repeated intratracheal exposures to one of four materials: (1) Hudson County chromium-contaminated soil (CCS), (2) CCS augmented with calcium chromate (CaCrO4), (3) CaCrO4 alone, or (4) control soil. Nominal total doses of Cr(+6) for each respective group were 324 microg/kg, 7,975 microg/kg, 8,700 microg/kg, and 0.02 microg/kg. Incidences of malignant tumors and nephritis were not elevated in any group. Four primary lung tumors appeared in animals that received CCS + CaCrO4, and one primary lung tumor appeared in the group treated with CaCrO4 alone. These incidences were not significant statistically, but the rare spontaneous occurrence of these tumors in Sprague-Dawley rats suggested that they were treatment related. No primary lung tumors appeared in the control or CCS-treated groups.

Animals↗