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Variations in total and ionized calcium during cardiac surgery.

Twenty patients undergoing cardiac surgery were studied to examine variations in total and ionized serum calcium and urine calcium during cardiopulmonary bypass. Serial samples of blood and urine were analyzed during bypass using a highly specific calcium electrode to determine the effects of hemodilution, various pharmacologic agents, and transfusions of citrated blood. Calcium chloride was routinely added to the crystalloid pump prime (400 mgs/L) and also administered when additional blood or crystalloid were infused. An average of 4.8 +/- .50 grams of calcium chloride was given per procedure. After induction of general anesthesia with nitrous oxide and Halothane, total serum calcium decreased from 10.0 +/- 0.3 to 8.5 +/- 0.8 mg% (p less than 0.05). Following heparinization, ionized calcium decreased from 4.2 +/- .08 to 3.9 +/- 12 mg% (p less than 0.05). Ionized calcium was not affected by reversal of heparin with Protamine. Following institution of cardiopulmonary bypass the ratio of ionized to total calcium declined about 13.4% (0.49 vs. 0.43). This ratio did not change during bypass but returned to normal immediately post-perfusion. Urinary calcium excretion averaged 1.9 +/- 0.6 mg/min and could not be implicated as a cause of hypocalcemia during bypass. Post-perfusion, ionized serum calcium rose 1.3 +/- .01 mg% for each gram of exogenously administered calcium chloride (p less than 0.05). From these observations, we conclude: (1) ionized and total serum calcium levels decreased significantly following institution of cardiopulmonary bypass alone, presumably as a result of hemodilution from the crystalloid pump prime and addition of citrated blood products; (2) induction of general anesthesia alone with nitrous oxide and Halothane is associated with a significant decrease in total serum calcium; (3) ionized calcium declined following heparinization but is unchanged by Protamine administration; (4) changes in total and ionized serum calcium are unaffected by urinary excretion during bypass; (5) exogenously administered calcium chloride significantly increases serum ionized calcium and these changes are inversely related to the circulating pool of calcium; (6) current protocols for administration of exogenous calcium chloride during bypass may result in insufficient levels of ionized calcium and we have adopted measures to correct these deficiencies, when indicated.

Calcium↗
PubMed2005

Regulation of calcium-activated chloride channels in smooth muscle cells: a complex picture is emerging.

Calcium-activated chloride channels (ClCa) are ligand-gated anion channels as they have been shown to be activated by a rise in intracellular Ca2+ concentration in various cell types including cardiac, skeletal and vascular smooth muscle cells, endothelial and epithelial cells, as well as neurons. Because ClCa channels are normally closed at resting, free intracellular Ca2+ concentration (approximately 100 nmol/L) in most cell types, they have generally been considered excitatory in nature, providing a triggering mechanism during signal transduction for membrane excitability, osmotic balance, transepithelial chloride movements, or fluid secretion. Unfortunately, the genes responsible for encoding this class of ion channels is still unknown. This review centers primarily on recent findings on the properties of these channels in smooth muscle cells. The first section discusses the functional significance and biophysical and pharmacological properties of ClCa channels in smooth muscle cells, and ends with a description of 2 candidate gene families (i.e., CLCA and Bestrophin) that are postulated to encode for these channels in various cell types. The second section provides a summary of recent findings demonstrating the regulation of native ClCa channels in vascular smooth muscle cells by calmodulin-dependent protein kinase II and calcineurin and how their fine tuning by these enzymes may influence vascular tone.

Animals↗
PubMed1994

CFTR and calcium-activated chloride currents in pancreatic duct cells of a transgenic CF mouse.

We have studied the cystic fibrosis transmembrane conductance regulator (CFTR) and calcium-activated chloride currents in pancreatic duct cells isolated from a transgenic cf/cf mouse created by targeted insertional mutagenesis. Adenosine 3',5'-cyclic monophosphate (cAMP)-activated CFTR chloride currents were detected in 78% (29/37) of wild-type cells, in 81% (35/43) of heterozygote cells, and in 61% (29/47) of homozygous cf/cf duct cells (P > 0.05, cf/cf vs. wild-type and heterozygote). The CFTR current density measured at membrane potentials of +/- 60 mV averaged 22-26 pA/pF in wild-type and heterozygote groups but only 13 pA/pF in cells derived from cf/cf animals (P < 0.05, cf/cf vs. wild-type and cf/cf vs. heterozygotes). In contrast, duct cells from animals of all three genotypic groups exhibited calcium-activated chloride currents that were of similar magnitude and up to 11-fold larger than the CFTR currents. We speculate that these transgenic insertional null mice do not develop the pancreatic pathology that occurs in cystic fibrosis patients because their duct cells contain 1) some wild-type CFTR generated by exon skipping and aberrant splicing and 2) a separate anion secretory pathway mediated by calcium-activated chloride channels.

Animals↗
PubMed1991

Comparison of inotropic and chronotropic responses in rat isolated atria and ventricles.

1. The positive inotropic and chronotropic responses to adrenoceptor agonists (noradrenaline, phenylephrine), to compounds which increase cAMP by post-adrenoceptor mechanisms (forskolin, theophylline and dibutyryl cAMP) and to calcium chloride were measured in isolated rat atria and papillary muscles from both ventricles. 2. Noradrenaline produced similar maximal inotropic responses to calcium chloride in all tissues. Forskolin gave similar responses to calcium chloride in atrial but not ventricular tissues; the reverse was observed with dibutyryl cAMP. Phenylephrine and theophylline produced significantly smaller inotropic responses than calcium chloride in all tissues, especially in ventricular tissues. 3. Maximal chronotropic responses to noradrenaline, theophylline and dibutyryl cAMP were similar. Forskolin produced significantly greater responses while calcium chloride and phenylephrine produced significantly smaller responses than noradrenaline. 4. These results show that the maximal positive inotropic response of some agonists is markedly dependent on the tissue chosen. Further, chronotropic responses in right atria do not mimic inotropic responses in left atria.

Animals↗
PubMed1988

Reversal of the adverse cardiovascular effects of intravenous diltiazem in anesthetized dogs.

Intravenous diltiazem can be used to treat myocardial ischemia, hypertension, and supraventricular dysrhythmias, but significant adverse effects including atrioventricular block and hypotension have been reported. At the present time, there is controversy as to which drug is most effective in reversing these sequelae. This study was designed to assess the effectiveness of calcium chloride v epinephrine in reversing these side effects. The hemodynamic and electrophysiologic effects of diltiazem infusion were investigated in eight dogs anesthetized with fentanyl and nitrous oxide/oxygen. This study confirmed that diltiazem infusions in high concentrations produced predominantly atrioventricular conduction depression followed by profound hypotension. Epinephrine infusion proved to be most effective in attenuating and eliminating each of these deleterious side effects. In contrast, calcium chloride did not significantly increase heart rate or blood pressure or reverse atrioventricular block. In two instances calcium chloride produced further depression of atrioventricular conduction, leading to severe bradycardia and sinus arrest. Although calcium chloride increased left ventricular contractile force (LV dP/ dt) and cardiac index (CI), mean arterial pressure was not affected and SVR was further decreased. This study indicates that calcium chloride should not be given to reverse the side effects of diltiazem in the presence of atrioventricular conduction block or profound hypotension. Calcium chloride is indicated only when isolated myocardial depression is present and after the calcium channels have been reopened by epinephrine.

Anesthesia↗
PubMed2005

Mixing behavior of 10-(perfluorohexyl)-decanol and DPPC.

Fluorocarbon alcohol such as 10-(perfluorohexyl)-decanol are of interest for novel pulmonary drug delivery approaches. The purpose of this study was to investigate the mixing behavior of 10-(perfluorohexyl)-decanol with dipalmitoylphosphatidylcholine (DPPC), the major component of lung surfactant as an aid in assessing usefulness for this and other biomedical applications. The impact of 10-(perfluorohexyl)-decanol on the phase transitions of DPPC bilayers fully hydrated with a 0.15 M sodium chloride solution were studied using differential scanning calorimetry (DSC). No peak corresponding to excess alcohol was observed. The fluorinated alcohol caused DPPC peak broadening, especially below X(DPPC) < 0.95, and elimination of the pretransition of DPPC at X(DPPC) approximately 0.91. The onset of the main phase transition remains constant down to X(DPPC) approximately 0.91, suggesting limited miscibility in the gel phase. Hydration of the 10-(perfluorohexyl)-decanol-DPPC mixtures with calcium chloride (2 mM) in place of sodium chloride did not alter the macroscopic phase behavior. In addition to the thermal properties, the miscibility of 10-(perfluorohexyl)-decanol in DPPC in monolayers at the air water interface was investigated on water, sodium chloride (0.15 M), calcium chloride (2 mM) or hydrochloric acid (pH 1.9) subphases. The concentration dependence of the onset pressure of the liquid-expanded to liquid condensed phase transition of DPPC showed a slight change with increasing mole fraction on all four subphases. The surface area-mole fraction diagrams of 10-(perfluorohexyl)-decanol and DPPC on water, sodium chloride and calcium chloride showed near ideal behavior with slight negative deviations at higher surface pressure. A more significant negative deviation was observed for the hydrochloric acid subphase. Overall, both the DSC and the monolayer studies suggest that 10-(perfluorohexyl)-decanol and DPPC are partially miscible in biological mono- and bilayers. The macroscopic phase behavior 10-(perfluorohexyl)-decanol-DPPC system is significantly different from the analogous hydrocarbon system, which is attributed to a less favorable packing of the partially fluorinated hydrophobic tails in the mono- and bilayer.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1978

[Prevention of ventricular fibrillation with the aid of protopine in animal experiments].

The anti-arrhythmic activity of protopin, quinidine and novocainamide infused intravenously as a preventive and relieving measure was studied in acute experiments on rats with calcium chloride and aconitic arrhythmia. In myocardial fibrillation induced by calcium chloride the contents in the rat heart of adrenalin, noradrenaline, dopa and dopamine were studied by spectrofluorimetry before and after the use of protopin. It was established that in the size of its minimum effective doses which arrest or prevent calcium chloride and aconitic arrhythmias in rats protopin is two to three times more potent than quinidine and novocainamide. The mechanism of the anti-arrhythmic effect of protopin in calcium chloride and aconitic arrhythmias is complex and is due to the suppression of the foci of heterotopic stimulation, decrease in excitability of the myocardial cells and normalization of the catecholamine content in the myocardium.

Alkaloids↗
PubMed1989

[A study on the formation of apatite crystallized with gel method].

About apatite produced with a silicahydro gel method using calcium nitrate (group I) or calcium chloride (group II) and a gelatin gel method by use of calcium nitrate (group III) or calcium chloride (group IV), the formative volume as well as the formative condition of a periodic-layered precipitate (Liesegang ring), the pH measurement, calculation of Ca/P ratio, an estimation of the chlorine ion, morphological observation with a scanning electron microscope, qualitative analyses by X-ray diffraction (identification, crystallite size, lattice imperfections, lattice constants) and the composition analysis by infrared absorption spectroscopy were carried out to elucidate the formation of apatite using the gel method. The result showed that there were no distinct differences between group I-II and group III-IV, and it is suggested that it is possible to form satisfact fluorapatite with a gel method using calcium chloride as well as calcium nitrate.

Apatites↗
PubMed1986

Calcium: limited indications, some danger.

Calcium chloride has been advocated since the 1920s for the resuscitation of asystole, electromechanical dissociation (EMD), and ventricular fibrillation. Reports of side effects and complications have been numerous. Studies of calcium assays following American Heart Association recommended dosages have shown dangerously elevated serum levels. Large retrospective clinical studies in Milwaukee and Tampa have found no evidence of improved survival with calcium chloride in asystole and EMD. A prospective randomized double-blind study comparing calcium chloride and saline controls in the Milwaukee Paramedic system for asystole and EMD using standard AHA protocols showed no statistically significant difference in resuscitation rates or long-term survival between the calcium and no-calcium groups for the rhythm of asystole. Although patients with EMD had statistically improved resuscitation rates when calcium chloride was given, only one of the patients survived to hospital discharge. Because of the low rates of resuscitation and long-term survival in patients presenting in asystole and EMD, proving that calcium chloride does not enhance survival would require large multicenter trials. However, since no controlled study has ever documented significant benefit, its routine use in asystole and EMD cannot be supported. Calcium has long been used in medical treatment of hypocalcemic and hyperkalemic states and should be administered in moribund patients who have the proper clinical history and clinical signs of hypocalcemia.

Animals↗
PubMed1990

GTP-binding proteins mediate noradrenaline effects on calcium and chloride currents in rat portal vein myocytes.

1. Membrane currents were recorded by a patch-clamp pipette technique in cultured cells from rat portal vein using the whole-cell mode. 2. Noradrenaline (NA, 10(-5) M) and phorbol-12,13-dibutyrate (PDBu, 10(-7) M) produced an increase in voltage-dependent inward current carried by barium (5 mM), but their effects were not additive. Calcium-activated chloride current was evoked by NA but not by PDBu. 3. The NA-induced increase in peak voltage-dependent inward current was inhibited by intracellular application of GDP-beta-S (10(-3) M) while the effect of PDBu was unchanged. GDP-beta-S blocked the NA-induced chloride current but had no effect on the caffeine-induced chloride current. 4. Inclusion of GTP-gamma-S (10(-5)-10(-4) M) in the pipette solution increased the voltage-dependent inward current and inhibited the NA- or PDBu-induced increase in peak current. GTP-gamma-S potentiated the effect of NA on calcium-activated chloride current. At higher concentrations (10(-3) M), GTP-gamma-S activated the chloride current and prevented the effects of NA or caffeine on this current. 5. The combination of 10(-5) M-aluminium chloride and 10(-2) M-sodium fluoride had an effect similar to that of high concentrations of GTP-gamma-S on both inward current and calcium-activated chloride current. In contrast, arachidonic acid (10(-3) M) had no effect on calcium and chloride conductances activated by NA. 6. Cells responded normally to NA after pre-treatment for 4-30 h with 10 micrograms ml-1 pertussis toxin (PTx). 7. It is concluded that the stimulation of calcium and chloride conductances by NA is mediated through activation of a PTx-insensitive GTP-binding protein. This effect may involve activation of phospholipase C enzyme and production of both D-myo-inositol 1,4,5-trisphosphate which depletes calcium stores and diacylglycerol which activates protein kinase C.

Animals↗
PubMed1994

Modulation of developmental cerebellar ornithine decarboxylase activity by lead-acetate.

The developing brain is particularly susceptible to the neurotoxic effects of lead exposure. The ontological profile of ornithine decarboxylase (ODC) activity in the cerebellum was examined following lactational exposure of rats to 0.2% lead acetate (Pb). Relative to controls, Pb-exposure induced ODC activity levels in a transient manner with a 50% increase at postnatal day (PND) 6, a 20% increase at PND 9, returning to control basal levels by PND 15. These effects were seen at exposure levels of Pb that did not alter the normal growth and body weight of either the lactating dam or the developing pups. Basal cerebellar ODC activity in homogenates was increased with addition of low concentrations of Pb acetate (0.01 microM and 0.1 microM), while concentrations of 1 microM or greater were inhibitory. The effects of Pb acetate on tissue ODC activity in vitro were not mimicked by the addition of calcium chloride. Unlike tissue ODC activity, incubation of these metals with a pure ODC protein preparation exhibited fluctuations in ODC activity possibly due to the ionic interactions of Pb or calcium chloride. Calcium homeostatic mechanisms appeared to be unchanged with Pb exposure, at this dose, in that neither 45Ca-uptake (both mitochondrial and microsomal) nor synaptosomal Ca(2+)-ATPase activity was altered. These data suggest that alterations in ODC activity may be indicative of subtle toxicant induced perturbations during early development. Although the precise mechanism by which Pb may induce ODC activity in developing tissue is unknown, our results suggest that Pb may specifically alter ODC activity via cytosolic interactions.

Age Factors↗
PubMed1988

Interaction of dietary calcium and chloride and the influence of monovalent minerals on eggshell quality.

Two experiments were conducted to determine the influence of dietary sodium and chloride on eggshell quality of leghorn hens. In the first, hens were fed for 4 wk diets containing three levels of calcium (2.0, 2.8, and 3.5%) and two levels of chloride (.25 and .86%) in a factorial arrangement of treatments involving four replicates of five hens/treatment. Neither chloride nor calcium significantly affected hen-day egg production or egg weight (P greater than .05); however, chloride decreased feed consumption and calcium increased body weight gain (P less than .05). Interactions of calcium and chloride were significant for eggshell strength (P less than .06) and eggshell thickness (P less than .05). Chloride decreased these measures of eggshell quality only for hens receiving 2.0% calcium, and calcium improved both measures only for hens receiving .86% chloride. Chloride decreased blood bicarbonate concentration and base excess (P less than .05), but did not affect blood pH and pCO2 (P greater than .05). The effect of dietary sodium and chloride on eggshells of hens receiving 2.0% dietary calcium was determined in a second experiment. Seven diets ranging from .18% sodium and .94% chloride to .76% sodium and .24% chloride were provided for 4 wk to five replicates of five hens/treatment. Dietary sodium and chloride levels did not affect hen-day egg production or egg weight (P greater than .05). Increasing the proportions of sodium relative to chloride decreased food intake but increased eggshell strength and thickness (P less than .01) and increased blood pH (P less than .05), bicarbonate concentration (P less than .01), and base excess (P less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1998

Calcium release and calcium-activated chloride channels in airway smooth muscle cells.

Rapid progress has been made in the determination of specific ion channels expressed in airway smooth muscle cells and their role in excitation-contraction coupling. The combination of molecular biology and molecular physiology has provided insight into the properties of voltage-dependent cation (calcium and potassium) channels and their regulation by excitatory and inhibitory signaling processes. In this brief review, we will focus on calcium release and calcium-activated chloride channels. The former channels mediate receptor-activated calcium release, and the latter channels are opened following this release event. Moreover, the discovery of spontaneous calcium release events, or "calcium sparks," in smooth muscle, suggests an unanticipated level of regulation. Intracellular calcium release can drive electrical activity by the activation of calcium-dependent sarcolemmal ion channels, including calcium-activated chloride channels. These channels activate briefly but undergo a rapid phosphorylation by calcium/calmodulin-dependent protein kinase, which uncouples channel activity from cytosolic calcium. The coupling between intracellular calcium release and depolarizing chloride currents represents a potentially important signaling system in airway smooth muscle.

Bronchi↗
PubMed1997

Calcium-activated chloride current in normal mouse sympathetic ganglion cells.

1. In rat sympathetic ganglion cells, axotomy induces the appearance of a depolarizing after-potential (ADP) produced by a calcium-activated chloride current. Here we report that this current is also present in normal sympathetic neurones from the mouse. 2. In an in vitro preparation of the superior cervical ganglion, an ADP was observed after spike firing in 50% of the cells studied with single-electrode current- and voltage-clamp techniques. 3. When the cells were voltage clamped at -50 mV in the presence of tetrodotoxin (TTX) and tetraethylammonium chloride (TEA), depolarizing jumps evoked inward calcium currents which were contaminated by outward chloride currents, followed by slowly decaying inward chloride tail currents. 4. The ADP and the inward tail currents disappeared when calcium was removed from the extracellular solution or when cadmium was added. 5. The reversal potential for the inward tail current was approximately -24 mV and was displaced in agreement with the Nernst equation for chloride when the extracellular NaCl was replaced by sucrose or sodium isethionate. The chloride channel blocker anthracene-9-carboxylic acid (9AC) inhibited both the ADP and the tail current. 6. Using intracellular injection of neurobiotin, we found that cells with shorter dendrites had larger ADPs. In axotomized ganglia practically all cells showed very pronounced ADPs. 7. We conclude that normal mouse sympathetic ganglion cells have a calcium-activated chloride current that generates an ADP. The channels responsible for this current are probably located in the dendrites.

Action Potentials↗
PubMed1996

Calcium-activated chloride currents and non-selective cation channels in a novel cystic fibrosis-derived human pancreatic duct cell line.

The modulation of ion fluxes across the plasma membrane of epithelial cells is central for fluid secretion and absorption. Their disruption can lead to pathological states. An example is cystic fibrosis (CF), a disease characterized by abnormal functioning of the cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-modulated chloride channel. Here we report the characterization of calcium-activated, DIDS sensitive chloride current and non-selective calcium-activated cation channels in a novel human pancreatic duct cell line (YHV-1) derived from a non-delta F508 mutation CF patient bearing a severe phenotype. Southern blot analysis of the CFTR gene indicates a distinct electrophoretic pattern for the region spanned by exons 15-24, a result presumably related to a mutation which has yet to be identified. In contrast to large calcium-activated chloride currents there were no cAMP-dependent CFTR-type chloride currents. Non-selective cation channels were blocked by intracellular ATP and activated by intracellular calcium and cAMP. We propose the cell line YHV-1 as a suitable model for studying pancreatic ion and fluid secretion alterations in CF.

Blotting, Southern↗
PubMed1999

ErbB2 and ErbB3 receptors mediate inhibition of calcium-dependent chloride secretion in colonic epithelial cells.

We have previously demonstrated that epidermal growth factor (EGF) inhibits calcium-dependent chloride secretion via a mechanism involving stimulation of phosphatidylinositol 3-kinase (PI3-K). The muscarinic agonist of chloride secretion, carbachol (CCh), also stimulates an antisecretory pathway that involves transactivation of the EGF receptor (EGFR) but does not involve PI3-K. Here, we have examined if ErbB receptors, other than the EGFR, have a role in regulation of colonic secretion and if differential effects on ErbB receptor activation may explain the ability of the EGFR to propagate diverse signaling pathways in response to EGF versus CCh. Basolateral, but not apical, addition of the ErbB3/ErbB4 ligand alpha-heregulin (HRG; 1-100 ng/ml) inhibited secretory responses to CCh (100 microM) across voltage-clamped T(84) epithelial cells. Immunoprecipitation/Western blot studies revealed that HRG (100 ng/ml) stimulated tyrosine phosphorylation and dimerization of ErbB3 and ErbB2, but had no effect on phosphorylation of the EGFR. HRG also stimulated recruitment of the p85 subunit of PI3-K to ErbB3/ErbB2 receptor dimers, while the PI3-K inhibitor, wortmannin (50 nM), completely reversed the inhibitory effect of HRG on CCh-stimulated secretion. Further studies revealed that, while both EGF (100 ng/ml) and CCh (100 microM) stimulated phosphorylation of the EGFR, only EGF stimulated phosphorylation of ErbB2, and neither stimulated ErbB3 phosphorylation. EGF, but not CCh, stimulated the formation of EGFR/ErbB2 receptor dimers and the recruitment of p85 to ErbB2. We conclude that ErbB2 and ErbB3 are expressed in T(84) cells and are functionally coupled to inhibition of calcium-dependent chloride secretion. Differential dimerization with other ErbB family members may underlie the ability of the EGFR to propagate diverse inhibitory signals in response to activation by EGF or transactivation by CCh.

Calcium↗
PubMed1977

Inhibition of carcinogenic effect of bracken fern (Pteridium aquilinum) by various chemicals.

The inhibitory effect of butylated hydroxyanosole (BHA), disulfiram, calcium chloride, and polyvinylpyrrolidone (PVP) on the intestinal and urothelial carcinogenicity of bracken fern (BF) was determined in albino rats. Of 10 groups of rats, one group received a normal diet, one received a BF-containing diet (one-third of diet by weight), four received a normal diet with one of the following supplements, and four received BF-containing diet with one of the following: BHA (5 mg/g diet); disulfiram (5 mg/g diet); PVP (50 mg/g diet); or calcium chloride (20 mg/g diet). At 12 months of the experiment, the following results were noted: in the BF-treated group, 30 rats (100%) exhibited intestinal tumors and 22 of 30 (73%) urinary bladder tumors. In the BF-BHA group, 15 of 20 rats (75%) showed intestinal tumors and 12 of 20 rats (60%) urinary bladder tumors. Of the 16 rats in the BF-disulfiram group, 12 (80%) had intestinal and 10 (62.5%) had urinary bladder tumors. In the BF-calcium chloride group, intestinal tumors arose in 16 of 23 rats (70%) and urinary bladder tumors in 4 of 23 rats (17%), while in the 28 BF-PVP rats, 26 (93%) exhibited tumors of the intestine and 5 (18%) tumors of the urinary bladder. Dietary BHA, disulfiram and calcium chloride decreased the incidence of intestinal tumors by about 25--30% (p less than 0.01). Similarly, PVP and calcium chloride inhibited BF-induced urinary bladder carcinogenesis by about 80% (p less than 0.001). No tumors were detected in groups receiving either normal diet or normal diet supplemented with BHA, disulfiram, calcium chloride or PVP.

Animals↗
PubMed1994

Action of niflumic acid on evoked and spontaneous calcium-activated chloride and potassium currents in smooth muscle cells from rabbit portal vein.

1. The action of niflumic acid was studied on spontaneous and evoked calcium-activated chloride (ICl(Ca)) and potassium (IK(Ca)) currents in rabbit isolated portal vein cells. 2. With the nystatin perforated patch technique in potassium-containing solutions at a holding potential of -77 mV (the potassium equilibrium potential), niflumic acid produced a concentration-dependent inhibition of spontaneous transient inward current (STIC, calcium-activated chloride current) amplitude. The concentration to reduce the STIC amplitude by 50% (IC50) was 3.6 x 10(-6) M. 3. At -77 mV holding potential, niflumic acid converted the STIC decay from a single exponential to 2 exponential components. In niflumic acid the fast component of decay was faster, and the slow component was slower than the control decay time constant. Increasing the concentration of niflumic acid enhanced the decay rate of the fast component and reduced the decay rate of the slow component. 4. The effect of niflumic acid on STIC amplitude was voltage-dependent and at -50 and +50 mV the IC50 values were 2.3 x 10(-6) M and 1.1 x 10(-6) M respectively (cf. 3.6 x 10(-6) M at -77 mV). 5. In K-free solutions at potentials of -50 mV and +50 mV, niflumic acid did not induce a dual exponential STIC decay but just increased the decay time constant at both potentials in a concentration-dependent manner. 6. Niflumic acid, in concentrations up to 5 x 10(-5) M, had no effect on spontaneous calcium-activated potassium currents. 7. Niflumic acid inhibited noradrenaline- and caffeine-evoked IO(Ca) with an ICM50 of 6.6 x 10-6 M, i.e.was less potent against evoked currents compared to spontaneous currents. In contrast niflumic acid(2 x 10-6 M-5 x 105 M) increased noradrenaline- and caffeine-induced IK(ca).8. The results are discussed with respect to the mechanism of block of ICl(Ca) by niflumic acid and its suitability as a pharmacological tool for assessing the role of Ic(ca) in physiological mechanisms.

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