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At least 703 records · Page 39Linked to original sources
PubMed1996

Insulin restores the calcium-activated chloride conductance in dedifferentiated renal glomerular mesangial cells from the H-2KB-TSA58 [corrected] transgenic mouse.

The effects of duration in culture were assessed in mesangial cells from the H-2Kb-tsA58 transgenic mouse using the whole-cell configuration of the patch clamp technique. The whole-cell potassium conductance remained constant in cells from passages 8-17 while the chloride conductance was found to decrease in cells after passage 15. This reduction of the chloride conductance, indicating cell dedifferentiation, was the result of complete loss of the calcium-activated component of the conductance and loss of part of the calcium-insensitive component. Insulin, which increases the calcium-sensitivity of the calcium-activated component of the chloride conductance in early passage cells, restored part of the calcium-sensitive component of the chloride conductance in dedifferentiated cells. Vasoactive agonists such as arginine vasopressin and angiotensin II stimulate a chloride-dependent depolarization in mesangial cells that initiates cell contraction. In view of the importance of the chloride flux it is possible that the loss of a significant magnitude of chloride conductance may underlie mesangial cell pathology to some degree. This is supported by data that show insulin can reverse many of the early renal changes observed in diabetic nephropathy and, as shown in this study, that insulin enhances the chloride conductance in dedifferentiated, cultured mesangial cells.

Animals↗
PubMed1993

Interplay between expressed non-NMDA receptors and endogenous calcium-activated chloride currents in Xenopus laevis oocytes.

Current-voltage (I-V) relationships of glutamate receptors activated by the non-NMDA receptor agonist, kainate (KA), were determined in Xenopus laevis oocytes injected with either calf or chick brain mRNA. In most injected oocytes (n = 44; 84%), I-V plots to 80 microM KA exhibited inward rectification; however, in some oocytes (n = 7; 16%), the KA-evoked membrane current showed only slight outward rectification. A comparison between the resting membrane properties of injected oocytes with the KA-evoked currents revealed that weak outward rectification was often observed in oocytes possessing predominant voltage-activated calcium-dependent chloride currents (ICl(Ca)). In these oocytes, replacement of extracellular calcium (2 mM Ca2+) with magnesium ions (Mg2+), or the addition of the chloride channel blocker, anthracene-9-carboxylic acid (500 microM to 1 mM A9C), reduced ICl(Ca) and also altered the nature of the KA I-V plot revealing inward rectification. It is proposed that the responses mediated by expressed non-NMDA receptors may be influenced by the activation of endogenous calcium-dependent membrane currents in Xenopus laevis oocytes.

Animals↗
PubMed2002

Suppressive effect of endogenous regucalcin on deoxyribonuclic acid synthesis in the nuclei of rat renal cortex.

The effect of regucalcin, a regulatory protein of Ca2+ signaling, on deoxyribonucleic acid (DNA) synthesis activity in the nuclei isolated from rat renal cortex was investigated. The addition of calcium chloride (10-100 microM) in the reaction mixture containing the nuclei caused a significant decrease in DNA synthesis activity. Nuclear DNA synthesis activity was significantly raised in the presence of EGTA (1 mM), a chelator of Ca2+, indicating that nuclear Ca2+ has an inhibitory effect. Regucalcin (0.1-0.5 microM) added in the reaction mixture in the presence of either EGTA (1 mM) or calcium chloride (50 microM) had a significant inhibitory effect on nuclear DNA synthesis activity. The presence of anti-regucalcin monoclonal antibody (10-50 ng/ml) in the reaction mixture caused a significant increase in DNA synthesis activity. This increase was completely abolished by the addition of regucalcin (0.5 microM). The effect of anti-regucalcin monoclonal antibody in increasing DNA synthesis was enhanced in the presence of EGTA. Additionally, an inhibitory effect of calcium chloride (10 or 50 microM) was enhanced in the presence of anti-regucalcin monoclonal antibody (25 ng/ml). The present study demonstrates that endogenous regucalcin has a suppressive effect on DNA synthesis in the nuclei of rat renal cortex.

Animals↗
PubMed1993

Plasma from normal pregnant women alters the reactivity of rabbit aortic smooth muscle with functional endothelium.

1. The effects of normal human pregnant plasma on the reactivity of rabbit aortic rings with documented endothelium have been studied. The rings were incubated in plasma from either normal pregnant or non-pregnant women and the effects of incubation on their responses to noradrenaline (NA), calcium chloride stimulation and potassium chloride-induced relaxation were examined. 2. There was no significant difference in the responses to NA in rings incubated in plasma from either pregnant or non-pregnant women. 3. The responses of the rings, incubated in both types of plasma, to calcium chloride stimulation through receptor-operated channels were similar, but rings incubated in plasma from pregnant women demonstrated decreased sensitivity and contractility to calcium chloride stimulation through voltage operated channels. 4. Potassium chloride-induced relaxation was significantly enhanced in rings incubated in plasma from normal pregnant women. The pattern of the responses was unaltered by either de-endothelialization or pretreatment of the rings with indomethacin. 5. The effects of plasma from pregnant women are similar to what has been reported as characteristic of vascular smooth muscle in normal pregnancy.

Animals↗
PubMed1996

Inhibition by P1075 and pinacidil of a calcium-independent chloride conductance in conditionally-immortal renal glomerular mesangial cells.

1. Depolarization of mesangial cells has been shown to occur following an outward movement of chloride ions from the cell. We have shown previously that mesangial cells from the H-2Kb-tsA58 transgenic mouse possess a significant whole-cell chloride conductance and consequently are a suitable preparation for the study of potential chloride channel inhibitors. 2. The effects on the whole-cell chloride conductance of the chloride channel inhibitor, 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB) and the potassium channel openers, (KCOs) P1075 and pinacidil were investigated in mesangial cells from the H-2Kb-tsA58 transgenic mouse cultured in permissive conditions (at 33 degrees C in the presence of 50 u ml-1 murine gamma-interferon). 3. In symmetrical solutions of 140 mM tetramethylammonium chloride (TMAC1) the whole-cell chloride conductance was 1.08 +/- 0.05 nS (n = 63) and this could be reversibly inhibited by 5 x 10(-5) M NPPB. 4. Both P1075 and pinacidil inhibited the whole-cell chloride conductance. This inhibition was not reversible after drug washout and was demonstrated only when drugs were applied to the extracellular surface of the cells. Very low concentrations of the drugs were found to reduce the chloride conductance after 16 h incubation but under no circumstances studied was the conductance totally inhibited, leaving a mean residual current of 0.33 +/- 0.03 nS (n = 12). 5. The effects of different peptide calcium concentrations on the magnitude of the residual current in the presence of the drugs were investigated. The residual current was reduced with 10(-8) M calcium in the pipette and increased with 10(-3) M pipette calcium. Therefore, these data suggest that P1075 and pinacidil selectively inhibit a calcium-independent chloride conductance in mesangial cells from the H-2Kb-tsA58 transgenic mouse.

Animals↗
PubMed1975

Effects of verapamil on the blood-perfused, isolated atrium preparation of the dog heart.

Thirteen isolated canine right atria were perfused with blood conducted from a support dog. The selective injection of verapamil into the cannulated sinus node artery at a dose level above 1 mug usually induced dose-dependent negative chronotropic and negative inotropic effects. At a dose of 30 mug, verapamil caused sinus arrest in 4 cases out of 7 with marked suppression of the isometric tension development. At 100 mug, in all cases it caused sinus arrest which continued about 1 hour. When calcium chloride was injected into the sinus node artery, a positive inotropic effect was dose-relatedly produced above a dose level of 100 mug, but the threshold dose for inducing a positive chronotropic effect of calcium chloride was approximately 1 mg. On the other hand, norepinephrine when injected into the sinus node artery simultaneously induced a positive chronotropic and inotropic effect at the same threshold dose. A dose level of 10-30 mug of verapamil did not significantly inhibit positive chronotropic and inotropic responses to norepinephrine and a positive inotropic response to calcium chloride in per cent. The negative inotropic response as well as the positive chronotropic and inotropic responses to electric stimulation of the epicardium were not blocked by verapamil which caused marked suppression of the tension development.

Alprenolol↗
PubMed1995

Activation of calcium-dependent chloride channels causes post-tetanic depolarization in rabbit parasympathetic neurons.

Intracellular recordings were made from neurons in rabbit and feline vesical parasympathetic ganglia in vitro. In response to cathodal current injection (0.1-1 nA for 2-20 ms) the majority of rabbit neurons (229 out of 250) exhibited a single action potential that was followed by a fast and slow after-hyperpolarization (sAHP neuron). The remainder of the cells exhibited an action potential followed by only a fast after-hyperpolarization (fAHP neuron). fAHP neurons did not exhibit anomalous rectification and a spontaneous rhythmic hyperpolarization, which were common membrane properties in sAHP neurons. In response to a train of cathodal current pulses (5-20 Hz for 0.1-10 s), fAHP neurons exhibited action potentials followed by a post-tetanic depolarization (PTD). The PTD was associated with a decrease in membrane input resistance. The amplitude and duration of the PTD were a function of the number of action potentials in the train. The amplitude of the PTD was increased by membrane hyperpolarization and its estimated reversal potential was approximately -30 mV. Low-chloride solution and intracellular injection of chloride ions augmented the amplitude and duration of the PTD, whereas low-sodium, high-potassium and low-potassium solutions did not affect them. Tetraethylammonium (5-10 mM) and barium (0.5-1 mM) increased the amplitude and duration of the PTD. Nominal calcium-free solutions and omega-conotoxin (500 nM) abolished the PTD. The data suggest that activation of chloride channels by calcium influx through omega-conotoxin-sensitive calcium channels mediates the PTD. Repetitive stimulation of the pelvic nerve evoked a train of orthodromic action potentials followed by the PTD of fAHP neurons. (+)-Tubocurarine (10 microM) and hexamethonium (200 microM), but not atropine (1 microM), abolished orthodromic action potentials and the PTD, whereas these cholinergic antagonists did not depress the PTD evoked by direct action potentials. In summary, the data suggest that the PTD may function as a slow synaptic potential in fAHP neurons. This appears likely because neither slow excitatory nor inhibitory postsynaptic potentials are present in neurons of rabbit vesical parasympathetic ganglia. In contrast, slow inhibitory and excitatory postsynaptic potentials were recorded from neurons in feline vesical parasympathetic ganglia.

Action Potentials↗
PubMed2003

Regulatory effect of regucalcin on nitric oxide synthase activity in rat kidney cortex cytosol: Role of endogenous regucalcin in transgenic rats.

The effect of regucalcin, a regulatory protein in Ca2+ signaling, on nitric oxid (NO) synthase activity in the cytosol of kidney cortex of rats was investigated. The presence of calcium chloride (10 micro M) in the enzyme reaction mixture caused a significant increase in NO synthase activity. This increase was significantly prevented by the addition of trifluoperazine (TFP; 20 or 50 micro M), an antagonist of calmodulin, supporting the existence of Ca2+/calmodulin-dependent NO synthase in rat kidney cortex cytosol. NO synthase activity was significantly decreased by the addition of regucalcin (10(-10)-10(-8) M) in the reaction mixture in the absence or presence of calcium chloride (10 micro M). The regucalcin (10(-8) M) effect was not seen in the presence of Nw-nitro-L-argine metylester (NAME; 10(-6) or 10(-5) M), an inhibitor of NO synthase. Regucalcin significantly reduced NO synthase activity in the presence of TFP (50 micro micro M) or EGTA (1 mM) which has a significant inhibitory effect on the enzyme activity. The presence of anti-regucalcin monoclonal antibody (25 or 50 ng/ml) in the reaction mixture caused a significant increase in NO synthase activity. This increase was completely abolished by the addition of regucalcin (10(-7) M). NO synthase activity was not significantly changed in the kidney cortex cytosol of regucalcin transgenic rats overexpressing endogenous regucalcin as compared with that of wild-type rats. However, the effect of calcium chloride (10 micro M) in increasing NO synthase activity in the kidney cortex cytosol of wild-type rats was significantly weakened in regucalcin transgenic rats. The present study demonstrates that endogenous regucalcin has a suppressive effect on NO synthase activity in the kidney cortex cytosol of rats.

Animals↗
PubMed1983

Responses of feline intradental sensory nerves to hyperosmotic stimulation of dentin.

The responses of intradental sensory nerves to hyperosmotic solutions of sucrose (4M) and calcium chloride (6M) applied in dentinal cavities were studied in anesthetized cats. Nerve impulse activity was recorded from canine teeth after application of the test solutions in shallow and deep cavities. In shallow cavities (thickness of remaining dentin, about 500 micron) sucrose and calcium chloride caused an immediate and transient excitation of the nerves in 3 out of 15 teeth and in 8 of 12 teeth, respectively. Treatment of such cavities with lactic acid (1M) increased the frequency of nerve responses to 100%. When applied in deep cavities (thickness of remaining dentin, 0-50 micron), sucrose induced a burst of impulses followed by continuous nerve activity, whereas calcium chloride decreased the nerve excitability. Our results support the hypothesis that solutions exerting an effective osmotic pressure excite the intradental nerves by an indirect mechanism when applied on the dentin and that they exert a direct effect on nerves when in contact with the pulp. In addition, it is suggested that acids produced in carious dentin may facilitate the induction of pain by hyperosmotic stimuli.

Action Potentials↗
PubMed2003

Preliminary pharmacological characterisation of an interleukin-13-enhanced calcium-activated chloride conductance in the human airway epithelium.

Interleukin (IL)-13 (10 ng/ml for 48 h) treatment of human bronchial epithelial cells induced a hypersecretory ion transport phenotype. Ussing chamber experiments demonstrated that this phenotypic change was characterised by an almost complete inhibition of the amiloride-sensitive short circuit current (ISC) and the appearance of an enhanced calcium-activated chloride conductance (CaCC). The peak increases in ISC (anion secretion) in response to UTP and ionomycin were increased by >8 fold and >13 fold respectively following IL-13 treatment. Changes in intra-cellular Ca(2+) levels following agonist exposure were not different between control and IL-13 treatments. The sensitivity of this IL-13-enhanced CaCC to several chloride channel-blocking molecules was determined following permeabilisation of the basolateral membrane and the establishment of a basolateral to apical chloride gradient. Under these conditions changes in ISC were regulated exclusively by the apical membrane and the current stimulated by ionomycin was sensitive to the chloride channel blockers diisothocyanatostilbene-2,2'-disulfonic acid (DIDS), dinitrostilben-2,2'-disulfonic acid (DNDS) and 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB) but was insensitive to tamoxifen. An understanding of the pharmacological profile of this conductance will ultimately aid in the determination of its molecular identity and function in the human airway epithelium.

Bronchi↗
PubMed1969

Complex-formation between triphosphoinositide and experimental allergic encephalitogenic protein.

1. Reactions between triphosphoinositide and the basic experimental allergic encephalitogenic (EAE) protein were examined in aqueous solution and in a biphasic solvent system (chloroform-methanol-water, 8:4:3, by vol.). 2. In the absence of salt an insoluble complex (I) is formed containing triphosphoinositide and EAE protein in proportions that represent complete neutralization of lipid and protein at the pH concerned. 3. In the presence of a low concentration (0.05m) of sodium chloride an insoluble positively charged complex (II) forms. It contains triphosphoinositide and EAE protein in a lower concentration ratio than complex I. This complex, which has a constant composition between pH7.5 and pH10, can take up additional micellar triphosphoinositide producing complex I, which can then be solubilized by excess of triphosphoinositide. 4. The complexes are dissociated by more concentrated sodium chloride solutions and low concentrations of calcium chloride, suggesting that they are largely stabilized by electrostatic bonds. The protein recovered after dissociation is immunologically active and has the same electrophoretic mobility as the original. 5. Water-insoluble ternary complexes containing triphosphoinositide, EAE protein and large amounts of phosphatidylcholine can be prepared. From these, chloroform-methanol (2:1, v/v) extracts only phosphatidylcholine. 6. An insoluble ternary complex of Ca(2+) ion, EAE protein and triphosphoinositide can be prepared by adding calcium chloride to a complex I preparation solubilized by excess of triphosphoinositide. 7. EAE protein will also form complexes with other acidic phospholipids, e.g. phosphatidic acid, phosphatidylserine and phosphatidylinositol, but not with phosphatidylcholine or phosphatidylethanolamine. The phosphatidylinositol and phosphatidylserine complexes are chloroform soluble, i.e. proteolipids. 8. The possibility that complexes between EAE protein and acidic phospholipids occur in vivo is discussed. Triphosphoinositide and EAE protein occur in ox brain myelin in approximately the same concentration ratios as they do in complex II, formed at physiological salt concentration and pH.

Animals↗
PubMed1978

Balance of net base in the rat. IV. Effects of oral calcium and phosphate loading.

Mineral and net base balances were studied in groups of male weanling Wistar rats given oral loads of calcium chloride, monocalcium phosphate plus monosodium phosphate, and disodium phosphate plus monopotassium phosphate, respectively. A group of adult nongrowing rats loaded with calcium chloride was included for comparison. In response to CaCl2 loading, gastrointestinal net base absorption was inhibited due, largely, to luminal precipitation of tertiary phosphates of calcium and magnesium. In the weanling animal, however, a rise in the rate of renal net acid excretion matched the concomitant decrement in the rate of net base absorption, permitting of continued skeletal net base storage. Similarly, in the adult animals augmented renal net acid excretion offset a positive rate of gastrointestinal net acid absorption with a resultant (normal) zero net base balance. Loading with monocalcium phosphate and disodium phosphate at a constant oral net base intake did not influence the overall net base balance, but disodium phosphate loading caused significant sodium retention.

Acid-Base Equilibrium↗
PubMed1989

Automated measurements of isolated heart muscle contractions: effects of halothane, calcium, and magnesium on guinea pig left atrial muscle.

An in vitro method for automatically measuring muscle contraction force has been demonstrated in a study of the effects of the inhalation anesthetic halothane followed by calcium chloride or magnesium sulfate on isolated guinea pig left atrial muscle. An automated computer-controlled system was used to collect muscle contraction force waveforms and to analyze contraction waveforms for comparison of variables before and after drug administration. Two concentrations of halothane (0.5 and 1.5%) were administered to the atrial preparation for 30 minutes and followed by calcium chloride or magnesium sulfate. Six variables (latency, time to peak tension, peak tension, maximum rate of change of pressure, force time integral, and relaxation time) were automatically determined from averaged stimulus-response curves. Results were normalized and compared with controls administered only calcium and magnesium and with controls administered no drugs. The automated system greatly simplified data collection and accumulation and statistical analysis of multiple responses. The system made possible averaging and analysis of more data with less variability than is normally obtained with manual systems. The results confirm several known actions of these agents. Halothane prolongs latency (9 and 21% for 0.5 and 1.5% halothane, respectively) and shortens time to peak tension (6 and 17% for 0.5 and 1.5% halothane, respectively) and relaxation time (17 and 39% for 0.5 and 1.5% halothane, respectively). At high halothane concentrations (1.5%) calcium chloride shortens latency (10%) and prolongs time to peak tension (11%); magnesium sulfate prolongs latency (14%) and shortens time to peak tension (10%).

Animals↗
PubMed1988

Effect of dietary calcium, phosphorus, chloride, and zeolite on the development of tibial dyschondroplasia.

The effect of synthetic zeolite was investigated on the development of tibial dyschondroplasia in young broilers fed diets in which the dietary levels of calcium, phosphorus, and chloride ranged from adequate to deficient. In the first two experiments the calcium level was maintained at .65% and four combinations were fed of .30% and .15% chloride and .75% and .50% phosphorus with and without 1% zeolite. Feeding the high phosphorus diet caused a high incidence of tibial dyschondroplasia that was lowered by feeding 1% zeolite. In both experiments the feeding of zeolite at a low level of dietary phosphorus caused a significant lowering of 16-day weight and bone ash. In the third experiment, when diets containing all combinations of .65% and .80% calcium and .50% and .60% phosphorus were fed, the addition of 1% zeolite caused a significant lowering of the 16-day weight, bone ash, and incidence, score, and percentage severe tibial dyschondroplasia. Once again as in the previous two experiments, there was a significant interaction between dietary phosphorus level and zeolite and 16-day weight and bone ash. Feeding zeolite significantly decreased phytate phosphorus retention.

Aluminum Silicates↗