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PubMed1985

[Antiarrhythmic action of 3-carbethoxyamino-5-dimethylaminoacetyl-iminodibenzyl hydrochloride (Bonnecor, AWD 19-166, GS -15) on experimental arrhythmia induced by aconitin, ouabain, calcium chloride and barium chloride].

In comparison with detajmium, prajmalium, ajmaline, quinidine, lidocaine, disopyramide, propranolol, and Ethmozin the substance GS 015 is tested on the aconitin-induced arrhythmia of the rat, the auricular fibrillation by aconitin of the dog, the ventricular arrhythmia induced by ouabaine of the dog, the arrhythmia caused by calcium chloride of the rat, and the arrhythmia induced by barium chloride of the rabbit. The particular qualities of effect in the special forms of arrhythmia are discussed in connection with the study of the antiarrhythmic action in case of coronary occlusion, with the increase of the electric fibrillatory threshold, and with the electrophysiologic tests.

Aconitine↗

PubMed1996

1 alpha,25-(OH)2-vitamin D3 analogs with minimal in vivo calcemic activity can stimulate significant transepithelial calcium transport and mRNA expression in vitro.

Several 1 alpha,25-(OH)2-vitamin D3 (1 alpha,25-(OH)2-D3) analogs have significant antiproliferative effects in vitro but do not elevate serum calcium in vivo. We tested whether the lack of a calcemic response of a vitamin D analog in vivo is due to its inability to stimulate intestinal calcium absorption by examining the effect of several such compounds on transepithelial calcium transport in the human colonic carcinoma cell line Caco-2. The relative stimulations of calcium transport by the four A-ring diastereomers of 1 alpha, 25-(OH)2-D3 (1 alpha,3 beta) and a 3 beta-bromoacetate analog (1 alpha,3 beta-BrAc) of the vitamin following 48-h treatment of cells at 10 nM were 1 alpha,3 beta (=100%), 1 alpha,3 alpha (+45.2%), 1 beta,3 beta (-15.6%), 1 beta,3 alpha (+6.5%), and 1 alpha,3 beta-BrAc (+50.6%). This was similar to the reported affinity of these compounds for the vitamin D receptor (VDR) and suggests that VDR binding predicts calcium transport. In contrast, three noncalcemic, sidechain- or D-ring-modified analogs of vitamin D, 1 alpha,25-(OH)2-16-ene-D3, 1 alpha,25-(OH)2-16-ene-23-yne-D3, and 1 alpha,25,28-(OH)3-D2 (at 10 nM for 48 h), showed a different relationship between VDR affinity (150, 60, and 63% of 1 alpha, 25-(OH)2-D3, respectively) and calcium transport (74.1, 126, and 10%, respectively). Elevated calcium transport was accompanied by higher 24-hydroxylase and calbindin D9k mRNA levels. The data demonstrate that although some vitamin D compounds cannot stimulate calcium transport due to an inability to interact with the VDR (e.g., 1 beta isomers), other factors, e.g., differential cellular metabolism, may account for variations in biological response in vivo to various vitamin D analogs.

Biological Transport↗

PubMed1998

Midkine induces histamine release from mast cells and the immediate cutaneous response.

Midkine is a product of a retinoic acid-responsive gene and exerts a variety of biological activities. The aim of our investigation is to determine whether human midkine have histamine-releasing effects on mast cells, and to show the evidence of the inflammation induced by midkine. Midkine induced histamine release from rat peritoneal mast cells with a rapid response in a dose-dependent manner. Extracellular calcium inhibited the histamine release induced by midkine in a dose-dependent manner. Pertussis toxin and benzalkonium chloride inhibited the histamine release induced by midkine. Gi-proteins exert an effect on the histamine release of midkine. The immediate cutaneous response induced by midkine was positive. These results suggest that midkine may take part in some inflammation via histamine release from mast cells.

Animals↗

PubMed1982

Arsenazo III and antipyrylazo III calcium transients in single skeletal muscle fibers.

The metallochrome calcium indicators arsenazo III and antipyrylazo III have been introduced individually into cut single frog skeletal muscle fibers from which calcium transients have been elicited either by action potential stimulation or by voltage-clamp pulses of up to 50 ms in duration. Calcium transients recorded with both dyes at selected wavelengths have similar characteristics when elicited by action potentials. Longer voltage-clamp pulse stimulation reveals differences in the late phases of the optical signals obtained with the two dyes. The effects of different tension blocking methods on Ca transients were compared experimentally. Internal application of EGTA at concentrations up to 3 mM was demonstrated to be efficient in blocking movement artifacts without affecting Ca transients. Higher EGTA concentrations affect the Ca signals' characteristics. Differential effects of internally applied EGTA on tension development as opposed to calcium transients suggest that diffusion with binding from Ca++ release sites to filament overlap sites may be significant. The spectral characteristics of the absorbance transients recorded with arsenazo III suggest that in situ recorded signals cannot be easily interpreted in terms of Ca concentration changes. A more exhaustic knowledge of the dye chemistry and/or in situ complications in the use of the dye will be necessary.

Animals↗

PubMed1981

Sister-chromatid exchanges induced by some chromium compounds in human lymphocytes in vitro.

Treatments with various concentrations of K2Cr2O7, CaCrO4 and CrO3 were given to human lymphocytes cultured in presence of BrdUrd for 2 replicative cycles. Sister-chromatid exchanges (SCEs) were visualized by a combination of fluorescent and Giemsa techniques. In all cases, the higher the concentrations the higher the frequencies of SCEs per metaphase and per chromosome. On a concentration basis, the order of effectiveness in producing SCEs was: CaCrO4 much greater than CrO3 greater than K2Cr2O7.

Bromodeoxyuridine↗

PubMed2001

Characteristics of a store-operated calcium-permeable channel: sarcoendoplasmic reticulum calcium pump function controls channel gating.

We examined the single channel properties and regulation of store-operated calcium channels (SOCC). In human submandibular gland cells, carbachol (CCh) induced flickery channel activity while thapsigargin (Tg) induced burst-like activity, with relatively lower open probability (NP(o)) and longer mean open time. Tg- and CCh-activated channels were permeable to Na(+) and Ba(2+), but not to NMDG, in the absence of Ca(2+). The channels exhibited similar Ca(2+), Na(+), and Ba(2+) conductances and were inhibited by 2-aminoethoxydiphenylborate, xestospongin C, Gd(3+), and La(3+). CCh stimulated flickery activity changed to burst-like activity by (i) addition of Tg, (ii) using Na(+) instead of Ca(2+), (iii) using Ca(2+)-free bath solution, or (iv) buffering [Ca(2+)](i) with BAPTA-AM. Buffering [Ca(2+)](i) induced a 2-fold increase in NP(o) of Tg-stimulated SOCC. Reducing free [Ca(2+)] in the endoplasmic reticulum with the divalent cation chelator, N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN), induced burst-like channel activity similar to that seen with CCh + Tg. Thus, SOCC is activated by stimulation of muscarinic receptors, inhibition of the sarcoendoplasmic Ca(2+) pump, and lowering [Ca(2+)] in the internal store. Importantly, SOCC activity depends on [Ca(2+)](i) and the free [Ca(2+)] in the internal store. These novel findings reveal that SERCA plays a major role in the gating of SOCC by (i) refilling the internal Ca(2+) store(s) and (ii) decreasing the [Ca(2+)](i)-dependent inhibition.

Barium↗

PubMed1997

Studies on ion channel antagonist-binding sites in sunflower protoplasts.

The cytological location of ion channel antagonist-binding sites was studied in sunflower protoplasts using the fluorescent probes DM-Bodipy-PAA and DM-Bodipy-DHP. The binding specificity of the probes was established by competition experiments with Bepridil, phenylalkylamine (Verapamil) and dihydropyridine (Nifedipine) which are known as calcium and potassium channel antagonists. Quantitative image analysis of the fluorescence emitted by the protoplasts showed the existence of interactions between PAA- and DHP-binding sites. Moreover, studies on the cytolocalization of the PAA receptors by confocal imaging showed that in freshly isolated protoplasts, DM-Bodipy-PAA binds exclusively at sites located in the cortical region of the cell.

Binding Sites↗

PubMed1979

Measurement of calcium influx under voltage clamp in molluscan neurones using the metallochromic dye arsenazo III.

1. The metallochromic indicator dye, arsenazo III, was injected into somata of molluscan neurones from Archidoris monteryensis. Membrane current and dye absorbance change were simultaneously monitored under voltage clamp. 2. Absorbance measured at 660 nm increased during positive-going voltage steps large enough to activate membrane conductances. In situ idifference spectra were qualitatively similar to dye, dye-calcium difference spectra recorded in vitro. The absorbance change was abolished by either a thorough removal of external calcium or internal chelation of calcium by EGTA. It was concluded that the absorbance increase primarily reflected changing internal calcium concentration and that the calcium entered from the outside. 3. Dye absorbance increased in a nearly linear fashion during voltage clamp pulses of 100--300 msec duration. This is in qualitative agreement with electrical stuidies which demonstrated only fractional inactivation of calcium conductance during such periods. Plots of absorbance change vs. Vm peaked at +30 to +40 mV and fell off sharply until approximately +70 mV where the slope became less steep. A null or reversal of the absorbance change was generally observed aroung +110 mV. Evidence is presented that calcium influx was in some cases sufficient to cause sizeable changes in its equilibrium potential. 4. During multisecond voltage clamps the slope of the absorbance change showed a large decline. Where barium substituted for calcium as the influx species in identical clamps, the absorbance at 660 nm also increased but in a much more linear fashion. Except for a slight effect on the initial few pulses, the absorbance signal did not recover after a period of barium influx. These results suggest that part of the slope decline might result from processes related to calcium uptake and not to membrane conductance decrease. 5. Dye absorbance changes during normal and TEA action potentials were measured. Comparison of these changes with voltage clamp records indicated that calcium influx during a spike was capable of raising concentration by roughly 2 X 10(-7) M if the cell were considered to be a uniform sphere with no buffering capacity. Calcium influx during action potentials was increased dramatically by TEA, primarily as a result of a prolonged plateau phase. The existence and duration of the plateau was controlled mainly by potassium conductance systems, however. There was no evidence found for facilitation of the calcium conductance. 6. Following a moderate influx of calcium it required 20--60 sec, depending on the neurone, for the dye absorbance to return to base line (at 9 degrees C). The recovery time course showed a marked difference when examined at different wavelengths. For lambda = 660 nm there was an initial period in which the absorbance decreased rapidly, followed by a slower phase which generally carried the absorbance below the initial (prepulse) value...

Action Potentials↗

PubMed1999

Pressure natriuresis in nitric oxide-deficient hypertensive rats: effect of antihypertensive treatments.

Chronic inhibition of nitric oxide (NO) synthesis has been shown to result in arterial hypertension and an important blunting of the pressure diuresis and natriuresis response (PDN). The mechanisms mediating these abnormalities are not completely understood. In the present study, the role of several antihypertensive drugs to ameliorate these alterations was evaluated. The PDN relationships have been evaluated in rats chronically (8 wk) treated with the NO synthesis inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME; 40 mg/kg per d in the drinking water). Appropriate groups of rats were simultaneously treated with the angiotensin II receptor blocker candesartan at a low (1.5 mg/kg per d) and high (2.5 mg/kg per d) dose, with the converting enzyme inhibitor captopril (60 mg/kg per d) and with the calcium channel blocker verapamil (100 mg/kg per d). Chronic treatment with L-NAME significantly elevated mean BP (163.6 +/- 6.5 mmHg versus 105.1 +/- 3.6 in controls), reduced GFR and renal blood flow (RBF), and shifted to the right the PDN responses. Chronic administration of low-dose candesartan, captopril, or verapamil prevented the arterial hypertension and improved renal hemodynamics, but these levels were not completely normalized. High-dose administration also improved renal hemodynamics but induced reduced BP below the levels of control animals. Despite the normalization of the elevated BP, the PDN responses of these hypertensive treated groups were not normalized, and the slopes of the respective diuretic or natriuretic responses were very similar to those of the hypertensive untreated rats. The results indicate that interruption or blockade of the renin-angiotensin system and calcium channel blockade are effective treatments for the NO-deficient arterial hypertension and renal vasoconstriction. However, the PDN responses are not normalized, and this finding suggests that the antihypertensive treatment is not enough to overcome the renal alterations associated with the chronic deficiency of NO.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2003

Control of acid gases using a fluidized bed adsorber.

During incineration, secondary pollutants such as acid gases, organic compounds, heavy metals and particulates are generated. Among these pollutants, the acid gases, including sulfur oxides (SO(x)) and hydrogen chloride (HCl), can cause corrosion of the incinerator piping and can generate acid rain after being emitted to the atmosphere. To address this problem, the present study used a novel combination of air pollution control devices (APCDs), composed of a fluidized bed adsorber integrated with a fabric filter. The major objective of the work is to demonstrate the performance of a fluidized bed adsorber for removal of acid gases from flue gas of an incinerator. The adsorbents added in the fluidized bed adsorber were mainly granular activated carbon (AC; with or without chemical treatment) and with calcium oxide used as an additive. The advantages of a fluidized bed reactor for high mass transfer and high gas-solid contact can enhance the removal of acid gases when using a dry method. On the other hand, because the fluidized bed can filter particles, fine particles prior to and after passing through the fluidized bed adsorber were investigated. The competing adsorption on activated carbon between different characteristics of pollutants was also given preliminary discussion. The results indicate that the removal efficiencies of the investigated acid gases, SO(2) and HCl, are higher than 94 and 87%, respectively. Thus, a fluidized bed adsorber integrated with a fabric filter has the potential to replace conventional APCDs, even when there are other pollutants at the same time.

Adsorption↗

PubMed2005

Extracellular group A Streptococcus induces keratinocyte apoptosis by dysregulating calcium signalling.

Group A Streptococcus (GAS) colonizes the oropharynx and damaged skin. To cause local infection or severe invasive syndromes the bacteria must gain access into deeper tissues. Host cell death may facilitate this process. GAS internalization has been identified to induce apoptosis. We now report an alternate mechanism of GAS-mediated apoptosis of primary human keratinocytes, initiated by extracellular GAS and involving dysregulation of intracellular calcium to produce endoplasmic reticulum stress. Two bacterial virulence factors are required for effective induction of apoptosis by extracellular GAS: (i) hyaluronic acid capsule that inhibits bacterial internalization and (ii) secreted cytolysin, streptolysin O (SLO), that forms transmembrane pores that permit extracellular calcium influx into the cytosol. Induction of keratinocyte apoptosis by wild-type GAS was accompanied by cell detachment and loss of epithelial integrity, a phenomenon not observed with GAS deficient in capsule or SLO. We propose that cell signalling initiated by extracellular GAS compromises the epithelial barrier by inducing premature keratinocyte differentiation and apoptosis, thereby facilitating GAS invasion of deeper tissues.

Apoptosis↗

PubMed2002

Calcium oscillations in freshly isolated neonatal rat cortical neurons.

AIM: To investigate the mechanisms of intracellular calcium concentration ([Ca2+]i) oscillations in freshly isolated neonatal rat cortical neurons. METHODS: Cortical neurons were isolated from neonatal rats 6-7 d after birth by enzymatic digestion. [Ca2+]i changes were measured in a microscopic calcium measurement system with Fura-2 as indicator. RESULTS: In a total of 82 neurons recorded, 47 showed spontaneous [Ca2+]i oscillations. The spontaneous [Ca2+]i oscillations were dependent on [Ca2+]o. Removal of [Ca2+]o completely abolished spontaneous oscillations. Tetraethylammonium 1 mmol/L increased both the amplitude and frequency of calcium oscillations, whereas the frequency was increased by Cs+ 1 mmol/L. Ba2+ 1 mmol/L, in contrast, induced [Ca2+]i oscillations superimposed on a sustained phasic increase. CONCLUSION: Spontaneous [Ca2+]i oscillation is an intrinsic property of neonatal rat cortical neurons. Potassium channels play an important role in the control of both the amplitude and frequency of [Ca2+]i oscillations in cortical neurons.

Animals↗

PubMed1991

Oscillating activity of a calcium-activated K+ channel in normal and cancerous mammary cells in culture.

Calcium-activated potassium channels were the channels most frequently observed in primary cultured normal mammary cell and in the established mammary tumor cell, MMT060562. In both cells, single-channel and whole-cell clamp recordings sometimes showed slow oscillations of the Ca2(+)-gated K+ current. The characteristics of the Ca2(+)-activated K+ channels in normal and cancerous mammary cells were quite similar. The slope conductances changed from 8 to 70 pS depending on the mode of recording and the ionic composition in the patch electrode. The open probability of this channel increased between 0.1 to 1 microM of the intracellular Ca2+, but it was independent of the membrane potential. Charybdotoxin reduced the activity of the Ca2(+)-activated K+ channel and the oscillation of the membrane current, but apamin had no apparent effect. The application of tetraethylammonium (TEA) from outside and BaCl2 from inside of the cell diminished the activity of the channel. The properties of this channel were different from those of both the large conductance (BK or MAXI K) and small conductance (SK) type Ca2(+)-activated K+ channels.

Animals↗

PubMed2006

Synthesis of 4-aryl-3,4-dihydropyrimidin-2(1H)-thione derivatives as potential calcium channel blockers.

Biginelli reaction which involves condensation of methyl 3-oxopentanoate, aromatic aldehydes and thiourea with a catalytic amount of HCl at reflux temperature has been used for the synthesis of 4-aryl-6-ethyl-5-(methoxycarbonyl)-3,4-dihydropyrimidin-2(1H)-thiones (1-16). In addition, Lewis acids such as FeCl(3).6H(2)O and/or H(3)BO(3) were also used as catalysts for one-pot synthesis of the products. Compared to the classical Biginelli reaction conditions, the usage of Lewis acids has the advantage of good yields and short reaction times. The calcium channel blocker activities of 1-16 were screened by the tests performed on isolated rat ileum and thoracic aorta. Although product 11, 2-nitrophenyl-derivative, has potent antispasmodic activity on BaCl(2)-stimulated rat ileum, it does not have vasodilator activity on KCl-stimulated rat thoracic aorta. Product 15, 2-ethoxyphenyl-derivative, exhibited significant antispasmodic and vasodilator activities in both screening paradigms.

Animals↗

PubMed1985

Mechanism of hydralazine-induced relaxation of arterial smooth muscle.

The effect of hydralazine on contractile responses by various agents has been studied in isolated rat tail artery strips. Hydralazine caused dose-dependent relaxation of contractions produced by 10(-7) mol.litre-1 noradrenaline (N); 10(-7) mol.litre-1 5-HT or 100 mmol.litre-1 KCl, suggesting that the relaxation response is non-specific. CaCl2 dose-response (in the presence of 10(-5) mol.litre-1 N; 10(-5) mol.litre-1 5-HT or 100 mmol.litre-1 KC1) was significantly inhibited by 5 X 10(-4) mol.litre-1 hydralazine in the order: KCl greater than 5-HT greater than N. Hydralazine also inhibited BaCl2 dose-response curve (in K+-depolarised strips); maximal contraction to BaCl2 was depressed by 87%. In other experiments, hydralazine significantly depressed (by 20%) the phasic contractile response to N due to mobilisation of calcium from a membrane-bound pool. D 600, a calcium entry blocker, also caused dose-dependent relaxation of contractile responses to all three agents studied; and inhibited CaCl2 and BaCl2 dose-response curves in K+-depolarised media, as well as depressed the phasic contractile response to N in Ca-free media by 17%. These results suggest that in the rat tail artery, hydralazine interferes with Ca2+ influx, as well as release from a membrane-bound pool.

Animals↗

PubMed1980

Laboratory studies of disinfectants against Legionella pneumophila.

Legionella pneumophila suspended in tap water was exposed to biocides recommended for inhibiting biological growth in cooling towers and evaporative condensers of air-conditioning systems. Chlorine, 2,2-dibromo-3-nitrilopropionamide, and a compound containing didecyldimethylammonium chloride and isopropanol were effective in destroying concentratiois of 10(5) to 10(6) viable cells per ml. Formulations consisting of 5-chloro-2-methyl-4-isothiazolin-3-one and 2-methyl-4-isothiazolin-3-one, disodium ethylene bis(thiocarbamate) and sodium dimethyl dithiocarbamate, and a phenolic with pentachlorophenate and sodium salts of other chlorophenols were less effective.

1-Propanol↗

PubMed2005

Calcium and chloride channel activation by angiotensin II-AT1 receptors in preglomerular vascular smooth muscle cells.

The pathways responsible for the rapid and sustained increases in [Ca(2+)](i) following activation of ANG II receptors (AT(1)) in renal vascular smooth muscle cells were evaluated using fluorescence microscopy. Resting intracellular calcium concentration [Ca(2+)](i) averaged 75 +/- 9 nM. The response to ANG II (100 nM) was characterized by a rapid initial increase of [Ca(2+)](i) by 74 +/- 6 nM (n = 35) followed by a decrease to a sustained level of 12 +/- 2 nM above baseline. The average time from peak to 50% reduction from the peak value (50% time point) was 32 +/- 4 s. AT(1) receptor blockade with 1 microM candesartan (n = 5) prevented the responses to ANG II. In nominally calcium-free conditions (n = 8), the peak increase in [Ca(2+)](i) averaged 42 +/- 7 nM but the sustained phase was absent and the 50% time point was reduced to 11 +/- 4 s. L-type calcium channel blockade with diltiazem reduced the peak [Ca(2+)](i) to 24 +/- 8 nM and the sustained level to 4 +/- 2 nM (n = 10). In cells preincubated in low Cl(-) (3.0 mM), the peak response to ANG II was suppressed as was the sustained response. Blockade of chloride channels with DIDS eliminated both the peak and sustained responses (n = 11); chloride channel blockade with DPC (n = 17) suppressed the peak increase in [Ca(2+)](i) to 18 +/- 5 and also prevented the sustained response. IP3 receptor blockade by 10 microM TMB-8 (n = 6) reduced the peak to 22 +/- 8 and prevented the sustained response. Exposure to 10 microM TMB-8 in the presence of Ca(2+)-free medium prevented the ANG II response (n = 9). In the presence of 100 microM DPC and 10 microM TMB-8 (n = 7), the ANG II response was also prevented. Thus the rapid initial increase in [Ca(2+)](i) is due not only to release from intracellular stores, but also to Ca(2+) influx from the extracellular fluid. Although Ca(2+) entry via L-type calcium channels is responsible for the major portion of the sustained response, other entry pathways participate. The finding that chloride channel blockers markedly attenuate both rapid and sustained responses indicates that chloride channel activation contributes to, rather than being the consequence of, the initial rapid response.

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

PubMed1995

Rational design and synthesis of small molecule, non-oligosaccharide selectin inhibitors: (alpha-D-mannopyranosyloxy)biphenyl-substituted carboxylic acids.

The calcium dependent E-selectin/sialyl Lewisx (sLex) interaction plays a key role in inflammation where it mediates the rolling of leukocytes prior to firm adhesion and extravasation from the vasculature. A model of E-selectin/sLex binding, along with previously reported structure-activity relationships of sLex-related oligosaccharide, was used in the rational design of non-oligosaccharide inhibitors of this pivotal interaction. A palladium-mediated biaryl-coupling (Suzuki) reaction was used as the key step to prepare a number of substituted biphenyls which were assayed for their ability to inhibit the binding of E-, P-, and L-selectin-IgG fusion proteins to sLex expressed on the surface of HL60 cells. Some of the compounds developed had greater in vitro potency than the parent sLex tetrasaccharide and are currently being evaluated in in vivo models of inflammation to select a candidate for clinical development.

Animals↗