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PubMed1991

Calcium and ethanol-induced gastric mucosal damage in rats.

The effects of graded doses of ethanol on stomach mucosal damage and calcium levels were studied in rats. The influence of verapamil and/or calcium chloride on these changes was also investigated. Orally administered ethanol (20, 50 or 80% v/v) markedly decreased gastric glandular tissue calcium and it concentration dependently produced mucosal lesions. Pretreatment with verapamil (2.5 or 5 mg/kg, i.p.) dose dependently lessened glandular wall calcium levels and worsened ethanol-induced mucosal damage. Calcium chloride (50 mg/kg, i.p.) significantly prevented ethanol-induced gastric calcium depletion; it also dose dependently antagonized the damaging effect of ethanol as well as the lesion-intensifying action of verapamil. The findings that verapamil potentiated, whereas calcium chloride prevented, ethanol-induced glandular mucosal damage and tissue calcium changes indeed suggest that altered gastric cell calcium levels could be closely related to the mucosal lesions produced by ethanol in rats.

Animals↗
PubMed1993

The role of endothelium in phenylephrine- and potassium-induced contractions of the rat aorta during pregnancy.

The involvement of endothelium in the contractile responses of rat aortic rings to phenylephrine and potassium chloride in pregnancy was examined. Contractions in response to both agents were significantly greater in rings from non-pregnant rats than in rings from pregnant rats, and they were unaltered by treatment of the rings with indomethacin. De-endothelialization potentiated the contractions of rings from pregnant rats in response to phenylephrine, but had no significant effect on similar rings contracted with potassium chloride. Whereas de-endothelialization had no significant effect on the contractions to phenylephrine in rings from non-pregnant rats, it decreased those of rings from the same type of rats, contracted with potassium chloride. Pregnancy significantly inhibited contractions in response to calcium chloride of rings treated with phenylephrine or potassium chloride. The effect of endothelium removal on contractions to calcium chloride in rings from pregnant and non-pregnant rats treated with phenylephrine or potassium chloride was similar to that observed for phenylephrine-induced and potassium chloride-induced contractions, respectively. Contractions of intact aortic rings from pregnant and non-pregnant rats to phenylephrine in calcium-free medium were similar. Results of the study suggest that the effect of pregnancy on the contractions of the rat aorta in response to phenylephrine and potassium chloride is at least partly mediated by the endothelium and is independent of prostaglandin synthesis. The endothelial factor involved in this effect appears to modulate contractions by interfering with calcium influx through the receptor-operated calcium channels and the voltage-operated calcium channels.

Animals↗
PubMed1998

Calcium-activated chloride conductance in a pancreatic adenocarcinoma cell line of ductal origin (HPAF) and in freshly isolated human pancreatic duct cells.

Using the whole-cell patch-clamp technique, a calcium-activated chloride conductance (CACC) could be elicited in HPAF cells by addition of 1 microM ionomycin to the bath solution (66 +/- 22 pA/pF;Vm + 60 mV) or by addition of 1 microM calcium to the pipette solution (136 +/- 17 pA/pF; Vm + 60 mV). Both conductances had similar biophysical characteristics, including time-dependent inactivation at hyperpolarising potentials and a linear/slightly outwardly rectifying current/voltage (I/V) curve with a reversal potential (Erev) close to the calculated chloride equilibrium potential. The anion permeability sequence obtained from shifts in Erev was I > Br >/= Cl. 4,4'-Diisothiocyanatostilbene disulphonic acid (DIDS, 500 microM) caused a 13% inhibition of the current (Vm + 60 mV) while 100 microM glibenclamide, 30 nM TS-TM-calix[4]arene and 10 microM tamoxifen, all chloride channel blockers, had no marked effects (8%, -6% and -2% inhibition respectively). Niflumic acid (100 microM) caused a voltage-dependent inhibition of the current of 48% and 17% (Vm +/- 60 mV, respectively). In freshly isolated human pancreatic duct cells (PDCs) a CACC was elicited with 1 microM calcium in the pipette solution (260 +/- 62 pA/pF; Vm + 60 mV). The presence of this CACC in human PDCs could provide a possible therapeutic pathway for treatment of pancreatic insufficiency of the human pancreas in cystic fibrosis.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2003

[Progress in research on the functions of calcium and chloride channels in vascular endothelial cells].

Endothelial cells (EC) lining the inner lumen of the blood vessels are rich in ion channels that constitute the basis of a unique signal transduction function of the cells. The abundance of calcium and chloride channels in the plasma membrane of these nonexcitable cells has raised questions in regard to their functional roles. This review presents evidence for the involvement of these channels in the endothelial cell functions, in an attempt to further explore the relationship between cardiovascular diseases and functional abnormalities of the ion channels.

Animals↗
PubMed2006

Novel conserved hydrolase domain in the CLCA family of alleged calcium-activated chloride channels.

Advanced protein structure prediction methods combined with structure modeling show that the mammalian proteins, described until now as calcium-activated chloride channels (CLCAs), appear in fact to be membrane anchored metal-dependent hydrolases, possibly proteases. A metallohydrolase structural domain was predicted, unexpectedly, in the CLCA sequences. The well-conserved active site in the modeled structure of this hydrolase domain allows the prediction of catalytic action similar to that of metalloproteases. A number of protein structure prediction methods suggest the overall fold of the N-terminal hydrolase domain to be most similar to that of zinc metalloproteases (zincins), notably matrixins. This is confirmed by analysis of the three-dimensional structure model of the predicted CLCA1 hydrolase domain built using the known structure of the MMP-11 catalytic domain. Fragments of CLCA1 corresponding to the modeled hydrolase domain were expressed in Escherichia coli, and the resulting proteins were readily refolded into monomeric soluble protein, indicating formation of stable independent domains. The homology model was used to predict putative substrate sequences. Homologs of mammalian CLCA genes were detected in the genomes of a vast array of multicellular animals: lower vertebrates, tunicates, insects, crustaceans, echinoderms, and flatworms. The hydrolase prediction is discussed in the context of published experimentally determined effects of CLCA proteins on chloride conductance. Altered proteolytic processing of full-length CLCA1 containing a mutation abolishing the predicted hydrolase activity is shown as initial experimental evidence for a role of the hydrolase domain in processing of mature full-length CLCA1. The hydrolase prediction together with the presented experimental data add to doubts about the function of CLCAs as chloride channels and strengthen the hypothesis of channel-activating and/or channel-accessory roles.

Amino Acid Sequence↗
PubMedDate not supplied

Transcutaneous delivery of levodopa: enhancement by fatty acid synthesis inhibition.

The present investigation aimed at evaluating the role of fatty acid synthesis inhibition in enhancing transcutaneous delivery of levodopa (LD). Rat epidermis was treated with ethanol and various doses of cerulenin (an inhibitor of fatty acid synthase enzyme system) for reducing the normal level of fatty acids. Calcium chloride (0.1 mM) and/or verapamil (1 microM) were coapplied to cerulenin treated skin in order to modulate duration of epidermal perturbation. These treated skin portions were used for estimation of altered triglyceride content (an indicator of fatty acid synthesis), differential scanning calorimetry (DSC) analysis, and in vitro permeation of LD. Plasma concentration of LD was monitored in rats following topical application of various transdermal formulations. Application of cerulenin (0.1 or 0.15 mM/7 cm(2)) to viable rat skin inhibited approximately 60% triglyceride synthesis with respect to control at 2 h. Coapplication of calcium chloride (0.1 mM) significantly increased this inhibition, whereas verapamil application reduced this effect. The decrease in triglyceride content reduced the enthalpy of the lipid endothermic transition. The in vitro permeation of LD was enhanced 3-fold across skin excised after treatment with cerulenin. LD did not permeate across normal skin. The effective plasma concentration (C(eff)) of LD was achieved within 3 h and maintained till 10 h by a single topical application of a carbidopa-levodopa combination (1:4) to ethanol-perturbed cerulenin-treated skin. Coapplication of calcium chloride reduced the time lag to achieve C(eff) to 2 h and maintained it till 24 h. A single transdermal LD (64 mg) patch formulated with calcium chloride (0.1 mM) and cerulenin (0.1 mM) dissolved in a propylene glycol:ethanol (7:3) mixture seems to offer a noninvasive approach for transcutaneous delivery of levodopa.

Administration, Cutaneous↗
PubMedDate not supplied

D2-like dopamine receptors promote interactions between calcium and chloride channels that diminish rod synaptic transfer in the salamander retina.

Activation of D2-like dopamine receptors in rods with quinpirole stimulates L-type calcium currents (ICa). This result appears inconsistent with studies showing that D2-like dopamine receptor activation diminishes rod signals in second-order retinal neurons. Since small reductions in [Cl-] can inhibit photoreceptor ICa, we tested the hypothesis that enhancement of ICa with the D2/D4 receptor agonist, quinpirole, increases calcium-activated chloride currents (ICl(Ca)) causing an efflux of Cl- from rods that would provide a negative feedback inhibition of ICa. In agreement with studies from Xenopus, quinpirole reduced rod input to second-order neurons of tiger salamander retina without significantly altering rod voltage responses. Quinpirole also diminished the amplitude of depolarization-evoked increases in [Ca2+]i measured with Fura-2 in rods, a finding consistent with inhibition of synaptic transmission from rods. Electrophysiological and Cl(-)-imaging experiments indicated ECl in rods is approximately -20 mV. Quinpirole enhanced ICl(Ca) and elicited an efflux of Cl- at the resting potential. A similar Cl- efflux was produced by extracellular replacement of 24 mM Cl- with CH3SO4- and this low Cl- solution inhibited Ca2+ responses to a similar degree as quinpirole did. When ICl(Ca) was inhibited with niflumic acid, quinpirole enhanced both ICa and depolarization-evoked increases in [Ca2+]i. Furthermore, with niflumic acid, quinpirole no longer inhibited rod inputs into horizontal and bipolar cells. These results suggest an initial enhancement of ICa by quinpirole is followed by a stimulation of Cl- currents, including ICl(Ca). The net result is a Cl- efflux that inhibits depolarization-evoked increases in [Ca2+]i and synaptic transmission from rods.

Ambystoma↗
PubMed1982

Cytotoxicity and mutagenicity of dimethylnitrosamine in mammalian cells (CHO/HGPRT system); enhancement by calcium phosphate.

The cytotoxicity and mutagenicity of dimethylnitrosamine (DMN) was determined in the CHO/HGPRT system. Metabolic activation of the promutagen was achieved by use of liver homogenate supernatant (S9) prepared from Aroclor 1254-induced Sprague-Dawley rats. The cytotoxic and mutagenic effects of DMN were enhanced by the inclusion of calcium chloride in the incubation mix, and this enhancement was dependent on the presence of sodium phosphate. Under conditions that yielded maximal activity (10 mM calcium chloride, 10 mM magnesium chloride, 50 mM sodium phosphate), an apparent calcium phosphate precipitate was observed. DMN activity increased with increasing amounts of S9 protein over the range of 0.3-3.0 mg/ml in the S9 mix and appeared to plateau at higher concentrations. The mutagenicity of DMN can be described as 110 mutants/10(6) cells per mM DMN per mg/ml S9 protein per hour.

Animals↗
PubMed2004

[Inhibitive effect on airway mucus overproduction with DNA vaccine based on xenogeneic homologous calcium-activated chloride channel in asthmatic mice].

OBJECTIVE: To observe the inhibitive effect on airway mucus overproduction with DNA vaccine based on human calcium-activated chloride channel 1 (hCLCA1) in asthmatic mice, who own mCLCA3 being xenogeneic homology of hCLCA1 in airway goblet cell. METHODS: The DNA vaccine was made with hCLCA1 gene inserted into pSecTag2B, and then BALB/c mice were vaccinated by i.m. once every two weeks. When serum antibody showed binding activity to mCLCA3 with ELISA analysis, asthma will be induced with ovalbumin in the vaccinated mice. To detect mucus production, lung sections were PAS stained and their MUC5AC mRNA levels were investigated by reverse transcription polymerase chain reaction (RT-PCR). Mice in control groups were injected with pSecTag2B/mCLCA3, pSecTag2B and saline, respectively. RESULTS: Antiserum of vaccine group after three times vaccination showed good binding activity to three mCLCA3 extracellular domains (ED), and the activity to N-terminal C-terminal ED was stronger than middle-ED. After induced to asthma, the number of goblet cell and MUC5AC mRNA level in vaccine group were lower than these in control group. CONCLUSION: hCLCA1 DNA vaccine can induce mouse to produce serum antibody binding itself mCLCA3, and thus airway mucus overproduction of asthmatic mouse is effectively inhibited.

Animals↗
PubMed1984

Effects of streptomycin and neomycin on the adrenal medulla of dogs.

The blocking effects of streptomycin and neomycin upon adrenal neurotransmission were studied in dogs. The pressor responses to splanchnic nerve stimulation (SNS) or 50 micrograms/kg nicotine were both blocked by 100 mg/kg but not by 50 mg/kg of the antibiotics injected systemically through the femoral vein. The effect was reversed by intravenous infusion of calcium chloride. The pressor response to SNS, but not that to nicotine, was blocked by the antibiotics injected into the adrenal gland through the adrenolumbar vein at doses up to 10 mg/kg. This effect was reversed by 50 micrograms/kg calcium chloride. Higher doses of antibiotics blocked the response to both stimuli, with only the response to nicotine being reversed by calcium chloride. These data indicate that streptomycin and neomycin block adrenal neurotransmission by interfering with calcium ions at pre- or pre-plus postsynaptic levels depending on the dose and route of administration.

Adrenal Medulla↗
PubMed2005

Effect of calcium and carbonate concentrations on anionic membrane fouling during electrodialysis.

A previous study on electrodialysis of calcium and carbonate high concentration solutions demonstrated that calcium migrated through the cation-exchange membrane (CEM) was blocked by the anion-exchange membrane (AEM) where it formed another fouling. The aim of the present work was to complete the identification of the deposit formed on AEM during electrodialysis and to characterize its physical structure at the interface of the membrane. No fouling was found on the anionic membranes treated without calcium chloride in presence of sodium carbonate, while membranes used during ED process of solutions containing calcium chloride and sodium carbonate were slightly fouled. A thin layer of precipitates was observed on the anionic membrane surface. The appearance of precipitates was typical of a crystalline substance. The size and form of crystal increased in proportion to the concentration of calcium chloride in solution. Large and cubic crystals were the best defined on the membrane treated at 1600 mg/L of CaCl2. The precipitate was identified as calcium hydroxide. However, this fouling was not found to affect significantly the electrical conductivity and the thickness of the membranes. Furthermore, the fouling formed was reversible.

Anions↗
PubMed1968

Lysosomal phospholipases A1 and A2 of bovine adrenal medulla.

1. [(32)P]Lecithin and [(32)P]phosphatidylethanolamine were prepared by incubating rat liver mince with [(32)P]phosphate. With these (32)P-labelled phospholipids conditions for the quantitative assay of phospholipase A activity were established. 2. The distribution of phospholipase A activity between subcellular fractions of the bovine adrenal medulla was determined. Phospholipases A(1) and A(2), with pH optima at 4.2 and 6.5 respectively, were found in the large-granule fraction. By means of sucrose-density-gradient centrifugation it was shown that both these phospholipases were localized in lysosomes. 3. Lysosomal phospholipase A(1) catalysed the hydrolysis of [(32)P]lecithin and [(32)P]phosphatidylethanolamine at the same rate. The enzymic activity was inhibited by 70% in the presence of 10mm-calcium chloride. 4. Lysosomal phospholipase A(2) catalysed the hydrolysis of [(32)P]phosphatidylethanolamine more rapidly than it hydrolysed [(32)P]lecithin. The hydrolysis of [(32)P]phosphatidylethanolamine, but not that of [(32)P]lecithin, by phospholipase A(2) was activated by 0.8mm-calcium chloride. However, the hydrolysis of both substrates was inhibited by 8mm-calcium chloride. 5. The significance of the presence of phospholipase activity in lysosomes is discussed in relation to the functions of lysosomes in general and in the adrenal medulla.

Adrenal Medulla↗
PubMed2005

Increased expression of the calcium-activated chloride channel hCLCA1 in airways of patients with obstructive chronic bronchitis.

BACKGROUND: Interleukin (IL)-9 and its effect on enhancing the human calcium-activated chloride channel 1 (hCLCA1) expression have been shown to induce mucin production. Increased expression of hCLCA1 may, in turn, contribute to mucus overproduction in chronic obstructive pulmonary disease (COPD) with a chronic bronchitis (CB) phenotype. OBJECTIVE: To determine the expression of IL-9, IL-9 receptor (IL-9R), hCLCA1 and mucoglycoconjugates in COPD. METHODS: Bronchial biopsies were obtained from six patients with obstructive CB and six healthy control subjects. IL-9, IL-9R and hCLCA1 expression were detected using immunohistochemistry. Additionally, in situ hybridization was performed to determine the expression of hCLCA1 messenger RNA. Mucin production was assessed using periodic acid-Schiff staining. RESULTS: There was a significantly higher number of IL-9 immunoreactive cells in the submucosa of patients with COPD than that of healthy control subjects (P<0.05). Also, a significant increase in the expression of IL-9R, hCLCA1 (protein and messenger RNA) and mucin (periodic acid-Schiff-positive cells) was noted in the bronchial epithelium of patients with COPD compared the control subjects (P<0.05). CONCLUSION: Increased expression of IL-9, IL-9R and hCLCA1 in the bronchial mucosa of patients with obstructive CB suggests that mucus overproduction in this disease may be, at least in part, due to hCLCA1.

Aged↗
PubMed2006

Relationship of intracellular free Ca2+ concentration and calcium-activated chloride channels of pulmonary artery smooth muscle cells in rats under hypoxic conditions.

To investigate the relationship between intracellular free Ca2+ concentration ([Ca2+]i) and calcium-activated chloride (Clca) channels of pulmonary artery smooth muscle cells (PASMCs) in rats under acute and chronic hypoxic conditions, acute hypoxia-induced contraction was observed in rat pulmonary artery by using routine blood vascular perfusion in vitro. The fluorescence Ca2+ indicator Fura-2/AM was used to observe [Ca2+]i of rat PASMCs under normal and chronic hypoxic condition. The effect of Clca channels on PASMCs proliferation was assessed by MTT assay. The Clca channel blockers niflumic acid (NFA) and indanyloxyacetic acid (IAA-94) exerted inhibitory effects on acute hypoxia-evoked contractions in the pulmonary artery. Under chronic hypoxic condition, [Ca2+]i was increased. Under normoxic condition, [Ca2+]i was (123.63 +/- 18.98) nmol/L, and in hypoxic condition, [Ca2+]i was (281.75 +/- 16.48) nmol/L (P<0.01). Under normoxic condition, [Ca2+]i showed no significant change and no effect on Clca channels was observed (P> 0.05). Chronic hypoxia increased [Ca2+]i which opened Clca channels. The NFA and IAA-94 blocked the channels and decreased [Ca2+]i from (281.75 +/- 16.48) nmol/L to (117.66 +/- 15.36) nmol/L (P<0.01). MTT assay showed that under chronic hypoxic condition NFA and IAA-94 decreased the value of absorbency (A value) from 0.459 +/- 0.058 to 0.224 +/- 0.025 (P<0.01). Hypoxia increased [Ca2+]i which opened Clca channels and had a positive-feedback in [Ca2+]i. This may play an important role in hypoxic pulmonary hypertension. Under chronic hypoxic condition, Clca channel may play a part in the regulation of proliferation of PASMCs.

Animals↗
PubMed1964

CALCIUM IN RELATION TO THE ACTIONS OF OUABAIN AND ADRENALINE ON THE HEART.

Isolated pairs of rabbit auricles have been observed in media containing 6, 24 or 75 mM-potassium, with corresponding reductions in sodium concentration. In 24 mM-potassium, adrenaline restored beating and excitability, as did calcium chloride, but ouabain had no effect. In 75 mM-potassium, adrenaline had no effect; calcium chloride caused a contracture; ouabain had no direct effect, but auricles which had been beating in the presence of ouabain contracted promptly on transfer to 75 mM-potassium. Left auricles, which do not beat spontaneously, were less sensitive to calcium and to ouabain. The results showed a membrane stabilizing action of calcium and an action on muscular contraction, and suggested that cardiac glycosides acted by causing accumulation of calcium at the activator site in the tissue.

Animals↗