[Nonspecific resistance in patients with chronic gastritis undergoing treatment by drinking a calcium-sodium chloride low-mineralized mineral water].
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Administration, Oral↗
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Modulation of calcium-dependent chloride secretion by basolateral SK4-like channels in a human bronchial cell line.
The human bronchial cell line16HBE14o- was used as a model of airway epithelial cells to study the Ca(2+)-dependent Cl(-) secretion and the identity of K(Ca) channels involved in the generation of a favorable driving force for Cl(-) exit. After ionomycin application, a calcium-activated short-circuit current ( I(sc)) developed, presenting a transient peak followed by a plateau phase. Both phases were inhibited to different degrees by NFA, glybenclamide and NPPB but DIDS was only effective on the peak phase. (86)Rb effluxes through both apical and basolateral membranes were stimulated by calcium, blocked by charybdotoxin, clotrimazole and TPA. 1-EBIO, a SK-channel opener, stimulated (86)Rb effluxes. Block of basolateral K(Ca) channels resulted in I(sc) inhibition but, while reduced, I(sc) was still observed if mucosal Cl(-) was lowered. Among SK family members, only SK4 and SK1 mRNAs were detected by RT-PCR. KCNQ1 mRNAs were also identified, but involvement of K(cAMP) channels in Cl(-) secretion was unlikely, since cAMP application had no effect on (86)Rb effluxes. Moreover, chromanol 293B or clofilium, specific inhibitors of KCNQ1 channels, had no effect on cAMP-dependent I(sc). In conclusion, two distinct components of Cl(-) secretion were identified by a pharmacological approach after a Cai2+ rise. K(Ca) channels presenting the pharmacology of SK4 channels are present on both apical and basolateral membranes, but it is the basolateral SK4-like channels that play a major role in calcium-dependent chloride secretion in 16HBE14o- cells.
Adaptation, Physiological↗
Detection and separation of two kinds of acidic arginine amidases from boar sperm using lima bean trypsin inhibitor and aprotinin affinity adsorptions.
Two kinds of acidic arginine amidase activity were found in boar sperm. One enzyme was separated by a treatment consisting of lima bean trypsin inhibitor (LBTI) affinity adsorption and elution. The other enzyme was separated by aprotinin affinity adsorption and elution through the same solutions as those used for first enzyme; the two enzymes provisionally named boar sperm acidic arginine amidases 1 (BSAA-1) and 2 (BSAA-2), respectively. The amidolytic activity of BSAA-1 was increased by high concentrations of calcium chloride, while the activity of BSAA-2 was independent of calcium chloride. Their behavior with LBTI and aprotinin, and profiles of their substrate specificities, were also different. The affinity of LBTI to BSAA-1 was approximately 14 times higher than that to BSAA-2.
Adsorption↗
A calcium-activated chloride channel (HCLCA1) is strongly related to IL-9 expression and mucus production in bronchial epithelium of patients with asthma.
BACKGROUND: One of the cardinal features of airway remodeling in asthma is mucus gland hyperplasia and mucus overproduction and hypersecretion. Recently, a calcium-activated chloride channel, HCLCA1, was described that is upregulated by IL-9 and thought to regulate the expression of soluble gel-forming mucins, such as MUC5A/C, a critical component of mucus in the airways. OBJECTIVE: We sought to examine the expression of HCLCA1 in bronchial biopsy specimens of asthmatic subjects compared with those of control subjects and to demonstrate its relationship with IL-9, IL-9 receptor (IL-9R), and markers of mucus production. METHODS: Bronchial biopsy specimens from asthmatic (n = 9) and control (n = 10) subjects were stained with periodic acid-Schiff to identify mucus glycoconjugates. IL-9- and IL-9R-positive cells were identified with immunocytochemistry, and HCLCA1 expression was detected by means of in situ hybridization with cRNA probes. RESULTS: We demonstrate significant increases in IL-9 (P <.001) and IL-9R (P <.05) immunoreactivity, as well as increased expression of HCLCA1 mRNA (P <.001), in the epithelium of asthmatic patients compared with that found in control subjects. There was also an increase in the number of mucusproducing cells in biopsy specimens from asthmatic subjects (P <.001). HCLCA1 mRNA was strongly and selectively colocalized with periodic acid-Schiff and IL-9R-positive epithelial cells. In particular, a strong positive correlation was observed between HCLCA1 mRNA expression and IL-9-positive (r = 0.69, P < 0.01) or IL9R-positive (r = 0.79, P <.01) cells. CONCLUSION: An upregulation of HCLCA1 in the IL-9- responsive mucus-producing epithelium of asthmatic subjects compared with that seen in control subjects supports the hypothesis that this channel may be responsible, in part, for the overproduction of mucus in asthmatic subjects. These preliminary findings suggest the inhibition of HCLCA1 may be an important new therapeutic approach to control mucus overproduction in chronic airway disorders.
Adult↗
Increased expression of interleukin-9, interleukin-9 receptor, and the calcium-activated chloride channel hCLCA1 in the upper airways of patients with cystic fibrosis.
OBJECTIVES/HYPOTHESIS: Mucus overproduction is commonly found in airway disease in patients with cystic fibrosis. Interleukin-9 (IL-9) has been shown to mediate airway hyper-responsiveness and mucus overproduction. Recently, the calcium-activated chloride channel hCLCA1 has been described to be upregulated by IL-9 and has been thought to regulate the expression of soluble gel-forming mucins. We sought to examine the expression of IL-9, interleukin-9 receptor (IL-9R), and hCLCA1 in the upper airway of patients with cystic fibrosis in comparison to healthy control subjects and to demonstrate the relationship of IL-9, IL-9R, and hCLCA1 expression with mucus production. STUDY DESIGN: Prospective design. METHODS: Biopsy samples from nasal polyps of four patients with cystic fibrosis, nasal mucosa of six patients with cystic fibrosis, sinus mucosa of eight patients with cystic fibrosis, and nasal mucosa of six healthy control subjects were stained with periodic acid-Schiff (PAS) to identify mucus glycoconjugates. IL-9, IL-9R, and hCLCA1 expression was determined by immunocytochemical study. RESULTS: We demonstrated significant increases in IL-9, IL-9R, and hCLCA1 immunoreactivity in the mucosa of patients with cystic fibrosis compared with that found in control subjects (P <.05). There were no significant differences between the different locations (nasal polyps, nasal mucosa, and sinus mucosa) in the patient group (P >.05). We also observed a significant increase in the number of mucus-producing cells in biopsy specimens from patients with cystic fibrosis in comparison to control subjects. A positive correlation was found between hCLCA1-positive cells and IL-9-positive cells (correlation coefficient [r] = 0.79, P <.05) or IL-9R-positive cells (r = 0.92, P <.05). Moreover, a positive correlation was also present between PAS-positive (mucus-producing) cells and hCLCA1-positive cells (r = 0.64, P <.05) or IL-9R-positive cells (r = 0.64, P <.05). CONCLUSIONS: Increased expression of IL-9 and IL-9R, as well as upregulation of hCLCA1, in mucus-overproducing epithelium of patients with cystic fibrosis supports the hypothesis that IL-9 contributes to mucus overproduction in cystic fibrosis. Expression of hCLCA1 may also be responsible, in part, for the overproduction of mucus. These preliminary findings suggest that hCLCA1 might be an interesting new therapeutic target to control mucus overproduction in airway disease in patients with cystic fibrosis.
Biopsy↗
Synergistic action of cyclic adenosine monophosphate- and calcium-mediated chloride secretion in a colonic epithelial cell line.
Vasoactive intestinal polypeptide (VIP) and the calcium ionophore A23187 caused dose-dependent changes in the potential difference and the short circuit current (Isc) across confluent T84 cell monolayers mounted in modified Ussing chambers. Both VIP and A23187 stimulated net chloride secretion without altering sodium transport. Net chloride secretion accounted for the increase in Isc. When A23187 was tested in combination with VIP, net chloride secretion was significantly greater than predicted from the calculated sum of their individual responses indicating a synergistic effect. VIP increased cellular cyclic AMP (cAMP) production in a dose-dependent manner, whereas A23187 had no effect on cellular cAMP. We then determined whether VIP and A23187 activated different transport pathways. Earlier studies suggest that VIP activates a basolaterally localized, barium-sensitive potassium channel as well as an apically localized chloride conductance pathway. In this study, stimulation of basolateral membrane potassium efflux by A23187 was documented by preloading the monolayers with 86Rb+. Stimulation of potassium efflux by A23187 was additive to the VIP-stimulated potassium efflux. By itself, 0.3 microM A23187 did not alter transepithelial chloride permeability, and its stimulation of basolateral membrane potassium efflux caused only a relatively small amount of chloride secretion. However, in the presence of an increased transepithelial chloride permeability induced by VIP, the effectiveness of A23187 on chloride secretion was greatly augmented. Our studies suggest that cAMP and calcium each activate basolateral potassium channels, but cAMP also activates an apically localized chloride channel. Synergism results from cooperative interaction of potassium channels and the chloride channel.
Calcimycin↗
Relationship between calcium-activated chloride channel 1 and MUC5AC in goblet cell hyperplasia induced by interleukin-13 in human bronchial epithelial cells.
BACKGROUND: Interleukin (IL)-13 has recently been reported as the major T-helper 2 cytokine involved in mucus overproduction and oversecretion in allergic airways. However, the relationship between human calcium-activated chloride channel-1 (hCLCA1) and MUC5AC induced by IL-13 in vitro has not been fully investigated. OBJECTIVES: The present study examines whether IL-13 induces the expression of hCLCA1 in normal human bronchial epithelial (NHBE) cells. We also investigated the relationship between hCLCA1 and MUC5AC expression and the development of goblet cell hyperplasia (GCH). METHODS: NHBE cells were isolated from human bronchi, and cultured with an air-liquid interface. hCLCA1 and MUC5AC gene and protein expression, as well as GCH were examined in the cells after exposure to IL-13. RESULTS: Incubation with IL-13 for 14 and 21 days increased the total number of epithelial cells, the number of periodic acid-Schiff (PAS)-stained epithelial cells, the number of goblet cells, as well as expression of mRNA and protein of hCLCA1 and MUC5AC. The number of goblet cells with secretory granules also increased after 21 days of incubation with IL-13. Niflumic acid, a chloride channel inhibitor, reduced mRNA expression of hCLCA1 and MUC5AC, and reduced the number of PAS-positive cells after incubation with IL-13. NHBE cells exposed or not to IL-13 expressed IL-13 receptor alpha(1) (IL-13Ralpha(1)), and an antibody to IL-13 Ralpha(1) also reduced the number of PAS-positive cells after exposure to IL-13. CONCLUSIONS: IL-13 might induce the expression of MUC5AC and hCLCA1 gene and protein in well-differentiated NHBE cells. These cells might also differentiate into goblet cells and become hyperplastic.
Adult↗
Vasoconstrictor responses induced by alpha-adrenoreceptor agonists before and after removal of the endothelial cells of dog mesenteric arteries.
The stainless cannula inserting method was used to investigate the effects of alpha-adrenoreceptor agonists (phenylephrine, alpha 1-agonist and xylazine alpha 2-agonist) and calcium chloride on isolated and perfused dog mesenteric arteries with and without saponin treatment. By intraluminal administration, phenylephrine and calcium chloride caused vasoconstriction in a dose-related manner whilst xylazine was without significant effect. After intraluminal treatment with 3 mg of saponin, the endothelia of the arteries were completely removed as confirmed by pathological examinations. Phenylephrine- and xylazine-induced responses were not influenced by saponin treatment whereas calcium chloride-induced constriction was significantly enhanced.
Adrenergic alpha-Agonists↗
Ionized calcium in human male and female reproductive fluids: relationships to sperm motility.
The levels of ionized calcium in seminal plasma were approximately 20% of the serum levels. In contrast, cervical mucus contained a level of ionized calcium similar to both serum and follicular fluid. Titration of seminal plasma and serum with increasing concentrations of calcium chloride indicated a 10-fold higher calcium-binding capacity for seminal plasma. In a random group of men under semen investigation, concentrations of ionized calcium and citrate in semen were inversely correlated (r = 0.732; P less than 0.001), an observation which was confirmed by studies of split ejaculates. These findings supported the contention that citrate is the major regulator of the levels of ionized calcium in seminal plasma and primarily responsible for maintaining the calcium gradient between the seminal plasma and cervical mucus. No significant relationship could be demonstrated between the levels of ionized calcium in the ejaculates and any of the motility characteristics of the spermatozoa in the same sample. Furthermore, the addition of increasing quantities of calcium chloride (0.16-20.00 mM) to washed spermatozoa had no major effects on their progressive motility. These data suggest that human spermatozoa are effective in maintaining an appropriate level of internal ionized calcium, necessary for normal motility, despite fluctuations in external calcium.
Ascitic Fluid↗
Characterization of the calcium and chloride [3H]glutamate binding site in crude synaptic membranes from human brain tissue.
1. The specific binding properties of [3H]glutamate to crude synaptic membranes (CSM) from postmortem human brain were studied. 2. Equilibrium binding analysis of [3H]glutamate binding to CSM from human brain cortex revealed a KD = 110 +/- 12 nM and a Bmax = 27 +/- 4 pmol/mg protein). 3. Calcium increased the number of binding sites, Bmax = 44 +/- 6 pmol/mg protein, without a significant change in the affinity constant, KD = 95 +/- 10 nM. 4. The dissociation constant of the [3H]glutamate bound to human CSM was 4.0 +/- 0.4 min-1 (n = 3). 5. The relative potencies of glutamate analogs and 2-amino-4-phosphonobutyric acid (APB) to compete for the glutamate binding sites, in human CSM, were glutamate > quisqualate = ibotenic acid > APB >> alpha-amino-3-hydroxy-5-methyl-4-isoxozolepropionate acid. 6. The glutamate specific binding in CSM from postmortem human brain was particularly rich in the gyrus hippocampus, nucleus accumbens, thalamus and frontal cortex. 7. This glutamate binding protein is related, probably, to a presynaptic neurosecretory pathway.
Adult↗
Calcium-dependent chloride currents elicited by injection of ethanol into Xenopus oocytes.
Electrophysiological techniques were used to study the response of native Xenopus laevis oocytes to intracellular injection and bath application of ethanol. Injection of ethanol produced dose-dependent transient inward currents accompanied by large current fluctuations, with estimated intracellular concentrations ranging from 10 to 300 mM. The response duration varied between 2 and 15 min, with an onset delay of 2-15 s. The inward current sometimes consisted of a fast and a slow component. Bath application of equivalent concentrations elicited similar but considerably smaller responses. The current showed a reversal potential of -20 +/- 10 mV, corresponding to an increase in chloride permeability. The response was eliminated in the presence of low chloride saline and was blocked by the chloride channel inhibitors SITS and DIDS. Ethanol responses were inhibited by the intracellular injection of the calcium chelator EGTA and were unaffected when the extracellular calcium was lowered. It is concluded that ethanol injection into Xenopus oocytes elicits a release of calcium from intracellular stores, which then activates an increased membrane permeability to chloride.
4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
[Effect of choline chloride and calcium pantothenate on neuromuscular pathology caused by the administration of triamcinolone].
On isolated phrenico-diaphragmal preparations of 17-days old and adult rats it is shown that introduction of triamcinolon (for 3 days in amounts of 1.4 mg/kg) results in disruption of the neuro-muscular transmission, manifesting itself in a less intensive reaction to exogenous acetylcholine and alpha-tubocurarine. Administration of choline chloride and calcium pantothenate following that of triamcinolon does away with these effects of the glucocorticoid.
Acetylcholine↗
Complexoproductive and antiheparin properties of low density lipoproteins (LDL). III. Interaction of low density lipoproteins (LDL) with synthetic polyanionic compounds.
Low density lipoprotein (LDL) form insoluble complex bonds with polymetacrylic and polyvinylsulphonic acids in the presence of calcium chloride. Quantity of arising complexes depends on the concentrations of LDL, acids and calcium chloride and on pH. These complexes dissociate solutions of sodium chloride, urea and guanidine hydrochloride.
Calcium Chloride↗
Calcium-activated chloride current in rabbit ventricular myocytes.
We have used the whole-cell patch-clamp technique to examine the ionic basis for a transient outward current in rabbit ventricular myocytes. High concentrations of intracellular calcium buffer prevented the current, isoproterenol increased it, and cadmium, nisoldipine, ryanodine, or caffeine blocked it. These data are consistent with a current that is calcium activated, by the calcium transient that causes contraction. The current was not blocked by external 4-aminopyridine or tetraethylammonium, and it was still present if external potassium was omitted and internal potassium was replaced by cesium. The current was absent when intracellular and extracellular chloride concentrations were drastically reduced, even when intracellular and extracellular potassium concentrations were normal. The current was blocked by the anion transport blockers 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid (SITS) and 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS) and responded to extracellular chloride changes as expected for a chloride current. We used SITS and DIDS to define the voltage dependence of the transient outward current. The current first appeared at voltages positive to the threshold of the calcium current and declined as voltage approached the calcium reversal potential. Tail-current experiments suggested that the current rectified strongly in the outward direction. We propose that the 4-aminopyridine-resistant transient outward current of rabbit ventricular myocytes is a calcium-activated chloride current.
4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
The effects of calcium supplementation of dairy cattle after calving on milk, milk fat and protein production, and fertility.
AIM: To determine the effect of calcium supplementation of dairy cattle after calving on serum concentrations of calcium, magnesium, and phosphorous after calving, and on reproductive and productive performance in the following lactation. METHODS: This was a double-blind randomised clinical trial using 356 dairy cows of parity 3 or greater from six seasonally calving commercial dairy herds. Cows were randomly assigned to a treatment and control group. The treatment group received two doses of 380 ml of calcium chloride in oil (49 g of elemental calcium); the first dose was given as soon as practical after calving and the second 12 hours later. Control cows received 380 ml of a placebo using the same treatment regime. Treatment and control cows had blood samples taken during the first 7 days after calving to determine serum calcium, magnesium and phosphorous levels. Treatment and control cows were monitored throughout the lactation to measure production and reproductive performance. RESULTS: Treatment had no effect on PSM to first service intervals. Treatment significantly reduced PSM to conception intervals in only one of the four herds with data available for analysis (p = 0.09). There was no difference between treatment groups for adjusted corrected milk yield calculated from the first herd test milk yield (p = 0.93) or 305-day milk solids production (p = 0.19). CONCLUSION: Further studies are required to identify reasons for the between-herd effectiveness of calcium chloride treatment in improving fertility.
Journal Article↗
Relaxation of guinea-pig stomach by bradykinin.
Intraluminal pressure changes were recorded from guinea-pig stomachs in vitro. Bradykinin (Bk) (0.4-9.6 nM) was generally found to produce a biphasic response (relaxation followed by contraction) in bathing solutions containing 1.1 mM calcium chloride. In bathing solutions containing 5.2 mM calcium chloride a relaxation without contraction was the most common observation. Relaxations to Bk were unaffected by selective concentrations of tetrodotoxin (5.6 microM), phentolamine (5.0-50.0 microM) and propranolol (5.0-50.0 microM). During virtually complete desensitization to Bk produced by 3 cumulative doses of 6.4 nM, relaxations to vagal stimulation were only reduced by 24.2% and those to adrenaline (2.0 microM) by 25.9%, indicating that Bk is unlikely to be the inhibitory transmitter released during vagal stimulation. Relaxations to ATP (10 microM) were reduced by 89.4% suggesting that Bk and ATP share a common step in the production of relaxation.
Animals↗
Glucose oxidase release from calcium alginate gel capsules.
Diffusion of glucose oxidase within calcium alginate gel capsules has been assayed and the experimental data fitted to a simple semi-empirical power equation, which is used to analyse the solute release from polymeric devices. It was found that an increase in the concentration of sodium alginate and calcium chloride gives rise to a reduction in the enzyme leakage. This was verified when glucose oxidase (GOD) diffusion percentages were compared in capsules with thicknesses of the same order of magnitude but obtained under different experimental conditions. So, the use of sodium alginate and calcium chloride solutions of concentrations 0.5% w/v and 2.6% w/v, respectively, lead to a diffusion percentage of 25 +/- 2. This percentage was reduced to 8 +/- 3 when sodium alginate and calcium chloride concentrations were fixed at 1% w/v and 4% w/v, respectively, even though the thicknesses of the capsules were of the same order of magnitude.
Journal Article↗
New method of treatment for dentin hypersensitivity by precipitation of calcium phosphate in situ.
The hydrodynamic theory is generally accepted as an explanation of hypersensitive dentin and suggests that occlusion of exposed dentinal tubules should result in a reduction of hypersensitivity. We tried to block tubules by in situ precipitation of insoluble calcium phosphate. Calcium phosphate crystals precipitated in situ on patent dentin surfaces and formed in the tubules immediately upon serial application of sodium phosphate and calcium chloride solutions, thus occluding the tubules. The size of crystals, their degree of coverage, and the thickness of the precipitate depended on the method of application and concentration of the solutions. The application of 5% disodium phosphate solution followed by rubbing with 10% calcium chloride solution resulted in immediate relief from dental hypersensitivity in 84% of patients treated.
Adult↗