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PubMed1986

Regional anticoagulation: hemodialysis with hypertonic trisodium citrate.

We have developed a simplified method for performing regional citrate anticoagulation during hemodialysis. High ultrafiltration rates and specialized equipment were obviated by the use of a 1.6-mol/L trisodium citrate solution and a standard calcium-containing dialysate. Thirty-six dialyses were performed with this technique on 14 stable and 22 high bleeding risk patients. There was no significant decline in plasma-ionized calcium during citrate dialysis, ie, 3.85 +/- 0.34 mg/dL (mean +/- SE) predialysis, to 3.31 +/- 0.26 postdialysis; furthermore, no patient developed neuromuscular symptoms or evidence of cardiovascular instability from hypocalcemia. Serum sodium rose with this procedure, but not to hypernatremic levels. This method of citrate dialysis is safe and effective during continuous blood flow (double-needle) hemodialysis, and is no more difficult to perform than conventional heparin dialysis. Single-needle (reciprocating blood flow) hemodialysis was successfully performed by the additional use of a calcium-free dialysate and separate calcium chloride infusion (10% calcium chloride), but risks the production of unexpected hypercalcemia.

Bicarbonates↗
PubMed1996

Cardiac preconditioning with calcium: clinically accessible myocardial protection.

Cardiac preconditioning is mediated by protein kinase C. Although endogenous calcium is a potent stimulus of protein kinase C, it remains unknown whether preischemic administration of exogenous calcium can induce protein kinase C-mediated myocardial protection against ischemia-reperfusion injury. To study this, calcium chloride was administered retrogradely through the aorta at a rate 5 nmol/min for 2 minutes to isolated perfused rat hearts 10 minutes before a 20-minute ischemia and 40-minute reperfusion insult. Calcium-mediated cardioadaptation was then linked to protein kinase C by means of the protein kinase C inhibitor chelerythrine (20 mumol.L-1.2 min-1). To determine whether exogenous calcium administration induces protein kinase C translocation and activation, immunohistochemical staining for the calcium-dependent protein kinase C isoform alpha was performed on adjacent 5 microns myocardial sections with and without calcium chloride treatment. Results indicated that preischemic calcium chloride administration improved myocardial functional recovery, as determined by enhanced developed pressure, improved coronary flow, reduced end-diastolic pressure, and decreased creatine kinase leakage during reperfusion. Beneficial effects of calcium chloride were eliminated by concurrent protein kinase C inhibition. Immunohistochemical staining for the alpha isoform of protein kinase C demonstrated that calcium chloride induces translocation of this isoform from the cytoplasm to the sarcolemma, indicating that exogenous calcium administration activates this isoform. These results suggest that calcium chloride, a safe and routinely administered agent, can induce protein kinase C-mediated cardiac preconditioning. Calcium-induced cardioadaptation to ischemia-reperfusion injury may be promising as a clinically feasible therapy before planned ischemic events such as cardiac allograft preservation and elective cardiac operations.

Alkaloids↗
PubMed1986

Effect of preload on rat aortic smooth muscle sensitivity to vasoactive agents.

Concentration-response curves to potassium chloride, phenylephrine, serotonin and calcium chloride were obtained from rat aortic strips subjected to preloads of 0.75, 1.5 or 3.0 g. The sensitivity of the aortic smooth muscle to potassium chloride, phenylephrine and serotonin increased with increasing preload; whereas the calcium chloride concentration-response curves of K+-depolarized strips were unaffected by preload. These results demonstrate that the sensitivity of rat aortic smooth muscle to many vasoactive agents is a function of preload and also indicate that an alteration in the influx of external Ca2+ is not sufficient to explain the effect of preload on sensitivity.

Animals↗
PubMed1977

Influence of magnesium on chloride-induced calcium release in skinned muscle fibers.

Chloride-induced Ca release in skinned muscle fibers was studied by measuring isometric force transients and 45Ca loss from fiber to washout solutions. Skinned fibers prepared from muscles soaked in normal Ringer solution made large force transients in 120 mM Cl solution with 5 mM ATP and 1 mM Mg, but 3 mM Mg was inhibitory. Mg inhibition was antagonized by low temperature and by Cd, agents which slow active Ca uptake by the sarcoplasmic reticulum (SR). In low Mg++, Cl stimulated rapid 45Ca release from the SR in sufficient amounts to account for the force response. The increased 45Ca release was inhibited by EGTA, suggesting that release requires free Ca under these conditions. The 45Ca initially released was partially reaccumulated later. Reaccumulation was increased in higher Mg++. These results provide additional evidence that the Ca uptake rate is an important determinant of net release, and suggest that Mg++ acts primarily on this mechanism. Skinned fibers prepared from muscles soaked in low Cl solutions could give force responses to Cl solutions with 3 mM and 6 mM Mg. This observation suggests that the Cl stimulus varies with the [Cl] gradient across the internal membranes, and supports the hypothesis that applied Cl causes membrane depolarization.

Animals↗
PubMed2004

Calcium-activated chloride channel-2 in human epithelia.

Calcium-activated chloride channels (CLCAs) are a family of multifunctional proteins that are widely distributed in tissues. To investigate the distribution of human CLCA-2 (hCLCA2) in human epithelia at the light and electron microscopic levels, we raised a primary antibody against a synthetic polypeptide sequence from natural hCLCA2. Corneal, skin, vaginal, esophageal, and laryngeal epithelia were immunopositive for hCLCA2 at the cytosolic aspect of the basal cells adjacent to the basement membrane. Epithelia of stomach and small intestine showed no hCLCA2 immunoreactivity. This study reports the cellular distribution of hCLCA2 in human epithelia and suggests its possible involvement in epithelial stratification and cell-substrate adhesion.

Chloride Channels↗
PubMed1997

Calcium effect on the membrane preparation of segmented poly(ether/urethane/amide) (PEUN) as a biomedical material.

Poly(ether/urethane/amide) (PEUN), a segmented polyurethane, was characterized concerning phase relationship, viscosity in solution, hydraulic permeability, mechanical properties, and in vivo biocompatibility with tissue and blood. PEUN was dissolved at the highest concentration of 0.5% in N,N-dimethylformamide (DMF). Addition of calcium chloride at concentrations up to 3.1% progressively increased the solubility of PEUN in DMF PEUN2 membrane was prepared by casting from mixtures of PEUN, 3% calcium chloride, and DMF, from which calcium chloride was sufficiently removed. The PEUN2 membrane thus obtained was compared with PEUN membrane which was prepared by casting from DMF solution without the addition of calcium chloride. The water permeability across PEUN2 membrane was higher than that across PEUN membrane. PEUN2 membrane in the swollen state exhibited a lower tensile modulus and much greater elastic property than PEUN membrane. Tissue compatibility of PEUN2 membrane was better than that of PEUN membrane. Thromboresistance of PEUN membrane was good, while PEUN2-coated surface was thrombogenic to some extent in vivo. Our characterization suggested that PEUN2 membrane is more hydrophilic than PEUN membrane, possibly because of the assembly of polar groups on the segments of PEUN molecules which show affinity to calcium chloride in membrane processing.

Animals↗
PubMed1988

Effects of hypercalcemia and ouabain on plasma atrial natriuretic polypeptide in anesthetized dogs.

For the purpose of examining the role of calcium ion in the secretory process of atrial natriuretic polypeptide (ANP), we studied the effects of hypercalcemia and ouabain on plasma concentration of immunoreactive ANP (irANP). Pentobarbital sodium-anesthetized dogs were treated with calcium chloride infusion (0.136 mmol.kg-1.min-1, 10 min) or ouabain injection (30 micrograms/kg), and plasma irANP concentration, right atrial pressure, mean arterial pressure, heart rate, and serum calcium concentration were measured. To evaluate the effect of rising arterial pressure, plasma irANP concentration was also measured in dogs treated with phenylephrine hydrochloride (10 micrograms/kg). With calcium chloride infusion, serum calcium concentration and plasma irANP concentration, respectively, increased to about three times and about four times their basal levels. This increase of plasma irANP concentration was not attenuated by pretreatment with adrenoceptor blockers. Ouabain increased plasma irANP concentration to approximately 2.5 times the initial level. Neither calcium chloride nor ouabain produced any effect on right atrial pressure and heart rate, but both significantly increased mean atrial pressure. Phenylephrine caused a greater increase in mean arterial pressure than both calcium chloride and ouabain. However, there was no significant increase in plasma irANP concentration. These results suggest that the calcium ion may play a key role in the secretory process of ANP.

Anesthesia, General↗
PubMed1993

Time course of spontaneous calcium-activated chloride currents in smooth muscle cells from the rabbit portal vein.

1. The time course of spontaneous calcium-activated chloride currents was studied with the perforated patch technique in freshly dispersed smooth muscle cells from the rabbit portal vein. 2. In potassium-containing solutions the spontaneous transient outward current (STOC, a calcium-activated potassium current) was more commonly recorded than spontaneous transient inward currents (STICs, a calcium-activated chloride current). In addition the duration of STOCs was much briefer (about 100 ms) than the duration of STICs (about 400 ms). 3. The decay of STICs could be described by a single exponential but the STOC decay appeared to be more complex. The decay time constant of STICs was not determined significantly by amplitude. 4. The time constant of decay of STICs (tau) was 86 ms at -50 mV and was increased by depolarization. Between -90 and +50 mV the relationship between tau and membrane potential was exponential and tau changed e-fold for a change of membrane potential of 120 mV. 5. The I-V relationship of STIC amplitude was linear between -10 and +50 mV but at more negative potentials the chord conductance was reduced and the I-V relationship exhibited negative slope conductance between -50 and -90 mV. 6. There was good agreement between the STIC tau values and the exponential relaxations to voltage steps evoked during caffeine-induced calcium-activated chloride currents. 7. In the presence of the chloride channel blocking agent anthracene-9-carboxylic acid the STIC amplitude was reduced and tau was increased. This effect was voltage dependent with a much greater effect at positive potentials. 8. The evidence suggests that the decay of STICs represents closure of chloride channels and tau approximates to the channel mean open time.

Animals↗
PubMed1996

Phosphatidylinositol 3-kinase mediates the inhibitory effect of epidermal growth factor on calcium-dependent chloride secretion.

Epidermal growth factor (EGF) and carbachol both inhibit calcium-activated chloride secretion by the human colonic epithelial cell line, T84. Although the inhibitory mechanism for the carbachol effect involves the 3,4,5,6-isomer of inositol tetrakisphosphate, the mechanisms responsible for the EGF effect have not yet been fully elucidated. Here, we studied the role of phosphatidylinositol 3-kinase (PI 3-kinase) in the inhibitory effect of EGF. The PI 3-kinase inhibitor, wortmannin, slightly increased basal chloride secretion and potentiated the secretory response to thapsigargin. Wortmannin also partially reversed EGF-induced, but not carbachol-induced, inhibition of thapsigargin-stimulated chloride secretion. Wortmannin alone had no effect on carbachol- or histamine-induced chloride secretion and completely reversed EGF-induced inhibition of the secretory response to these agonists. EGF, carbachol, histamine, and thapsigargin all increased levels of the 85-kDa regulatory subunit of PI 3-kinase in antiphosphotyrosine immunoprecipitates. However, only EGF significantly increased levels of the 110-kDa catalytic subunit. Furthermore, only EGF increased PI 3-kinase activity in an in vitro kinase assay. High levels of phosphatidylinositol (3)-monophosphate were present in unstimulated cells and significantly reduced by wortmannin. EGF, but not carbachol, rapidly increased levels of phosphatidylinositol (3,4)-bisphosphate and phosphatidylinositol (3,4,5)-trisphosphate. Production of these lipids was also sensitive to wortmannin. Our data suggest that EGF activates PI 3-kinase and that its lipid products may mediate the inhibitory effect of EGF on calcium-dependent chloride secretion. Our data also suggest that a phosphatidylinositol-specific 3-kinase activity is present in unstimulated T84 cells and may regulate production of phosphatidylinositol (3)-monophosphate and basal secretory tone.

Androstadienes↗
PubMed2000

Improving permissive infection of human cytomegalovirus in cell culture.

Changes in human cytomegalovirus (HCMV) titre occurring under different conditions were studied using plaque assay. No significant change in titre was found using primary embryonic fibroblasts or primary foreskin fibroblasts, or with the addition of dexamethasone to the medium. Significant increases in titre were found when standard cultures were pre-incubated in medium containing DEAE-dextran and/or calcium chloride. However, DEAE-dextran and/or calcium chloride had no significant effect on HCMV detection using the shell vial assay, possibly because enhancement affects permissive infection, but not surface expression of viral antigens. DEAE-dextran and calcium chloride can be included in the medium of standard cultures as a means of obtaining higher titres of HCMV, and are particularly useful for isolates that are difficult to culture.

Calcium Chloride↗
PubMed1994

Isolation and partial characterization of calcium-activated chloride ion channels from thylakoids.

The goal of the present work was to characterize the thylakoid anion channel. Toward this purpose a new, more sensitive, assay was developed to measure chloride channel activity of solubilized and partially purified thylakoid membrane proteins. In this assay potassium channel function was reduced or eliminated by the use of cesium as the coion of chloride. Under these conditions calcium but not magnesium stimulated anion uptake, suggesting the presence of a calcium-activated anion channel in isolated thylakoid membrane proteins. A polyclonal antibody raised against an anion channel isolated from epithelial membranes immunoreacted with three thylakoid membrane proteins; a doublet in the 62 to 66-kDa range and a single band in the 57 to 59-kDa region suggesting that the thylakoid anion channel may be homologous to the mammalian chloride channel. Furthermore, the cDNA which encodes the epithelial chloride channel hybridized on Northern blots prepared from corn total RNA with three mRNA bands.

Biological Transport↗
PubMed2004

A cyclic GMP-dependent calcium-activated chloride current in smooth-muscle cells from rat mesenteric resistance arteries.

We have previously demonstrated the presence of a cyclic GMP (cGMP)-dependent calcium-activated inward current in vascular smooth-muscle cells, and suggested this to be of importance in synchronizing smooth-muscle contraction. Here we demonstrate the characteristics of this current. Using conventional patch-clamp technique, whole-cell currents were evoked in freshly isolated smooth-muscle cells from rat mesenteric resistance arteries by elevation of intracellular calcium with either 10 mM caffeine, 1 microM BAY K8644, 0.4 microM ionomycin, or by high calcium concentration (900 nM) in the pipette solution. The current was found to be a calcium-activated chloride current with an absolute requirement for cyclic GMP (EC50 6.4 microM). The current could be activated by the constitutively active subunit of PKG. Current activation was blocked by the protein kinase G antagonist Rp-8-Br-PET-cGMP or with a peptide inhibitor of PKG, or with the nonhydrolysable ATP analogue AMP-PNP. Under biionic conditions, the anion permeability sequence of the channel was SCN- > Br- > I- > Cl- > acetate > F- >> aspartate, but the conductance sequence was I- > Br- > Cl- > acetate > F- > aspartate = SCN-. The current had no voltage or time dependence. It was inhibited by nickel and zinc ions in the micromolar range, but was unaffected by cobalt and had a low sensitivity to inhibition by the chloride channel blockers niflumic acid, DIDS, and IAA-94. The properties of this current in mesenteric artery smooth-muscle cells differed from those of the calcium-activated chloride current in pulmonary myocytes, which was cGMP-independent, exhibited a high sensitivity to inhibition by niflumic acid, was unaffected by zinc ions, and showed outward current rectification as has previously been reported for this current. Under conditions of high calcium in the patch-pipette solution, a current similar to the latter could be identified also in the mesenteric artery smooth-muscle cells. We conclude that smooth-muscle cells from rat mesenteric resistance arteries have a novel cGMP-dependent calcium-activated chloride current, which is activated by intracellular calcium release and which has characteristics distinct from other calcium-activated chloride currents.

Animals↗
PubMed2004

Molecular and functional analyses of two new calcium-activated chloride channel family members from mouse eye and intestine.

Two new calcium-activated chloride channel (CLCA) family members, mCLCA5 and mCLCA6, have been cloned from mouse eye and intestine, respectively. mCLCA5 is highly homologous to hCLCA2, and mCLCA6 is highly homologous to hCLCA4. mCLCA5 is widely expressed with strong expression in eye and spleen, whereas mCLCA6 is primarily expressed in intestine and stomach. mCLCA6 is also expressed as a splice variant lacking exon 8 and part of exon 10 in intestine and stomach. Transfection of tsA201 cells with enhanced green fluorescent protein-tagged versions of the three cDNAs reveals protein products of 155 and 65 kDa for mCLCA5 and mCLCA6 and 145 and 65 kDa for the mCLCA6 splice variant. In vitro translation of mCLCA5 generates a 90-kDa protein that does not appear to be glycosylated. mCLCA6 also generates a 90-kDa protein that is glycosylated to a 110-kDa product, whereas the mCLCA6 splice variant generates an 80-kDa product that is 100 kDa after glycosylation. Treatment of enhanced green fluorescent protein-tagged mCLCA6 with PNGase F (peptide: N-glycosidase F) to remove N-linked glycosyl groups shows a reduction in size of the 65 kDa product to 60 kDa. Consistent with the hypothesis that mCLCA5, mCLCA6, and its splice variant encode calcium-activated chloride channels, in HEK293 cells expressing CLCAs ionomycin-evoked increases in intracellular calcium stimulated a current that reversed near Cl(-) equilibrium potential, E(Cl). Furthermore, these currents were inhibited by the chloride channel blocker niflumic acid. Given the prominent role of hCLCA2 in cancer cell adhesion and the unique high level of expression of hCLCA4 in brain, the identification of their murine counterparts presents the opportunity to clarify the role of CLCAs in disease and normal cell physiology.

Amino Acid Sequence↗
PubMed2002

Molecular and functional characterization of a murine calcium-activated chloride channel expressed in smooth muscle.

To identify the gene products responsible for the calcium-activated chloride current in smooth muscle, reverse transcription-PCR with degenerate primers was performed on mouse intestine and other organs. A new member of the CLCA gene family was identified, mCLCA4, that is expressed preferentially in organs containing a high percentage of smooth muscle cells, including intestine, stomach, uterus, bladder, and aorta. Reverse transcription-PCR using template RNA prepared from mouse bladder and stomach smooth muscle layers dissected free of mucosa yielded mCLCA4-specific bands. In situ hybridization with an mCLCA4-specific probe confirmed prominent expression in smooth muscle of major vessels of the heart but not cardiac muscle. High expression was also detected in the gastrointestinal tract, in bronchioles, and in aortic and lung endothelial cells. Transient expression of mCLCA4 in 293T cells resulted in the appearance of a prominent calcium-activated chloride current. Whole-cell currents activated by ionomycin or methacholine were anion-selective and showed minimal rectification or voltage-dependent gating. Similar to endogenous currents in smooth muscle cells, methacholine-induced currents were transient, and spontaneous transient inward currents were occasionally observed at resting membrane potentials. These results link calcium-activated chloride channels in smooth muscle with a gene family whose members have been implicated in cystic fibrosis, cancer, and asthma.

Amino Acid Sequence↗
PubMed1974

Compatibility of trypsin-modified human erythrocytes in the rubella hemagglutination-inhibition test employing three serum treatment procedures.

Results of comparative tests using trypsin-modified human type O erythrocytes and cells from newly hatched chickens with three standard serum treatment methods for rubella hemagglutination-inhibition techniques are reported. The kaolin, heparin-manganous chloride and dextran sulfate-calcium chloride methods could all be used with both cell types. Reproducibility with heparin-manganous chloride and dextran sulfate-calcium chloride was excellent with both cell types. Both methods gave generally higher antibody titers than the kaolin procedure. However, the use of human cells resulted in a more sensitive system than chicken cells with all serum treatment methods.

Animals↗
PubMed1996

Analysis of the time course of calcium-activated chloride "tail" currents in rabbit portal vein smooth muscle cells.

The time course of calcium-activated chloride "tail" currents (Itail) in single cells of the rabbit portal vein was studied. These currents were activated by the influx of calcium through voltage-dependent calcium channels (VDCCs). At -50 mV, Itail decayed exponentially with a time constant (tau) of 80-100 ms that was independent of amplitude and was similar to the tau of the decay of spontaneous transient inward currents (STICs; calcium-activated chloride currents). The decays of the STIC and Itail had a similar voltage dependence between -50 and -110 mV and were similarly affected by the chloride channel blocker, niflumic acid. However, at more positive potentials (-20 to +40 mV), Itail was sustained for the duration of the test pulse in most cells, in contrast to STICs which decayed exponentially. At very positive potentials (e.g. +100 mV), when little calcium enters the cell through VDCCs, Itail decayed exponentially. Measurement of calcium current (ICa) at various potentials showed that the VDCCs did not inactivate fully at potentials between -20 and +30 mV. We propose that at negative potentials the decay of Itail is determined by slow gating of the chloride channel, but at positive potentials a sustained Itail is produced by persistent influx of calcium through non-inactivating VDCCs.

Animals↗
PubMed1992

Low dose calcium administration increases mortality during septic peritonitis in rats.

Calcium is essential for normal cellular function. However, increases in cell calcium are also involved in cellular dysfunction and death by activating destructive enzymatic processes such as proteases, nucleases, and lipases. Since ionized hypocalcemia is common during sepsis, calcium is often administered in an attempt to normalize circulating levels. Previous studies using endotoxin and large amounts of calcium demonstrated increased mortality in calcium-treated animals. This study extends these preliminary data to endogenous sepsis (cecal ligation) and low dose calcium therapy. Sprague Dawley rats (n = 9 per group) had jugular catheters placed and their cecums ligated. They were randomized to an infusion of D5W at 1 ml/hr, calcium chloride at 4 mg/ml/hr (Low Ca), or calcium chloride at 6 mg/ml/hr (High Ca) for 24 hr. An additional group of animals received calcium chloride at 6 mg/ml/hr but had no surgery. Animals were followed for 24 hr survival. A separate group of animals (n = 6 per group) was prepared in a similar manner. Blood was obtained 6 hr following cecal ligation for circulating endotoxin concentrations, and animals were sacrificed. Calcium infusion increased ionized calcium levels slightly (low Ca, 1.12 +/- .06 to 1.21 +/- .09; high Ca, 1.06 +/- .04 to 1.16 +/- .05; P less than 0.05). Survival (24 hr) was 100% in the nonseptic controls and D5W septic animals, 67% in the low Ca septic group, and 44% (P less than 0.05) in the high Ca septic group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Membrane depolarization in NRK fibroblasts by bradykinin is mediated by a calcium-dependent chloride conductance.

The effects of the phosphoinositide-mobilizing agonist bradykinin (BK) on membrane potential and intracellular calcium in monolayers of normal rat kidney (NRK) fibroblasts were investigated. BK induced a rapid transient depolarization in these cells, which was mimicked by other phosphoinositide-mobilizing factors such as prostaglandin F2alpha (PGF2alpha), lysophosphatidic acid (LPA), platelet-derived growth factor (PDGF-BB), and serum. Depolarization by BK was independent of extracellular Ca2+ or Na+. It was shown using extracellular Cl- substitutions that the depolarization was caused by an increased Cl- conductance. Depolarization was inhibited by 5-nitro-2-3-phenylpropyl(amino)benzoic acid (NPPB), niflumic acid, and flufenamic acid, inhibitors of calcium-dependent chloride channels. The depolarization provoked by BK could be mimicked by raising intracellular calcium with ionomycin or thapsigargin and could be blocked with geneticin, a blocker of phospholipase C. When intracellular calcium was buffered by loading the cells with 1,2-bis(2-aminophenoxy)ethane-NNN'N'-tetra-acetic acid (BAPTA), depolarization was prevented. We conclude that in NRK fibroblasts extracellular stimuli that increase intracellular calcium, depolarize the cells via the activation of a calcium-dependent chloride conductance. In addition to an increase in intracellular calcium, depolarization may be an important effector pathway in response to extracellular stimuli in fibroblasts. It is hypothesized that, in electrically coupled cells such as NRK fibroblasts, intercellular transmission of these depolarizations may represent a mechanism to coordinate uniform multicellular responses to Ca2+-mobilizing agonists.

Animals↗