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Calan (Verapamil Hydrochloride)
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Calan

Calan is in a group of drugs called calcium channel blockers. Calan is used to treat hypertension, angina and certain heart rhythm disorders. It works by relaxing the muscles of your heart and blood vessels.

Other names for this medication:

Similar Products:
Cartia XT, Cardizem, Cardizem LA, Nifedical XL , Propranolol, Procardia, Procardia XL

 

Also known as:  Verapamil Hydrochloride.

Description

Calan is in a group of drugs called calcium channel blockers. Calan is used to treat hypertension, angina and certain heart rhythm disorders.

It works by relaxing the muscles of your heart and blood vessels.

Calan is also known as Verapamil, Calaptin, Isoptin, Verelan, Bosoptin, Covera-HS.

Dosage

Take Calan orally.

Do not take Calan in large amounts.

Do not crush, chew, break, or open a controlled-delivery or extended-release tablet or capsule.

Swallow the whole pill.

It is important to use verapamil regularly to get the most benefit.

If you want to achieve most effective results do not stop taking Calan suddenly.

Overdose

If you overdose Calan and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Calan overdosage: slow heartbeat, fainting fit.

Storage

Store at room temperature between 15 and 25 degrees C (59 and 77 degrees F) away from moisture, light and heat. Keep container tightly closed. Keep out of the reach of children.

Side effects

The most common side effects associated with Calan are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Calan if you are allergic to Calan components.

Be careful with Calan if you're pregnant or you plan to have a baby, or you are a nursing mother.

Do not take Calan if you have poor heart condition, low blood pressure, recent heart attack.

Be careful with Calan if you suffer from kidney, liver disease, congestive heart failure, muscular dystrophy.

Be careful with Calan if you take medications such as any other blood pressure medications; buspirone (BuSpar); carbamazepine (Carbatrol, Tegretol); cimetidine (Tagamet, Tagamet HB); cyclosporine (Gengraf, Neoral, Sandimmune); digoxin (digitalis, Lanoxin, Lanoxicaps); lithium (Eskalith, LithoBid); lovastatin (Mevacor); phenobarbital (Solfoton); rifampin (Rifadin, Rimactane, Rifater); theophylline (Elixophyllin, Theo-24, Uniphyl); a sedative such as midazolam (Versed) or triazolam (Halcion); an antibiotic such as clarithromycin (Biaxin), erythromycin (E-Mycin, E.E.S., Ery-Tab, Erythrocin), fluconazole (Diflucan), itraconazole (Sporanox), ketoconazole (Nizoral), telithromycin (Ketek), or voriconazole (Vfend); a beta-blocker such as atenolol (Tenormin), bisoprolol (Zebeta, Ziac), metoprolol (Lopressor, Toprol), propranolol (Inderal, InnoPran), sotalol (Betapace), timolol (Blocadren), and others; a heart rhythm medication such as amiodarone (Cordarone, Pacerone), disopyramide (Norpace), flecainide (Tambocor), or quinidine (Quinaglute, Quinidex, Quin-Release); HIV/AIDS medicine such as amprenavir (Agenerase), atazanavir (Reyataz), delavirdine (Rescriptor), fosamprenavir (Lexiva), indinavir (Crixivan), nelfinavir (Viracept), or ritonavir (Norvir, Kaletra).

Do not use potassium supplements or salt substitutes.

Avoid eating grapefruit or drinking grapefruit juice while taking Calan.

If you want to achieve most effective results without any side effects it is better to avoid alcohol.

Be very careful when you are driving machine.

Do not stop taking Calan suddenly.

calan 180 mg

The increased transcription of jefA leads to increased resistance to ethambutol and isoniazid in M. tuberculosis via efflux pump like mechanism and contributes in the development of resistance to these drugs. JefA amino acid sequence is well conserved among clinically important bacterial genera, which further provides evidence of being a potent drug efflux pump. The involvement in drug resistance and very little homology with any of the human proteins makes JefA important to be included in the list of potential drug targets.

calan 240 mg

Our study aimed at evaluating the pharmacokinetic, cardiovascular, and metabolic effects of high-dose verapamil continuous intravenous infusion in cancer patients.

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Abstracts of trials were reviewed independently by 2 members of the study team. We reviewed English-language abstracts of non-English-language publications to assess qualitative consistency with our results.

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Clinical and experimental studies demonstrate that calcium (Ca2+) overload in myocardial cells is an important factor in the genesis of various serious arrhythmias. Calcium antagonists block voltage-dependent channels and thus reduce entry of Ca2+ into heart cells. Because of their specificity for atrioventricular nodal cells, verapamil and diltiazem are used clinically to treat supraventricular arrhythmias involving transmission in the atrioventricular node. These two drugs and the dihydropyridine (DHP) calcium antagonists have been shown to prevent ventricular ischemic and reperfusion arrhythmias in the laboratory. Despite these data indicating that calcium antagonists are antiarrhythmic, a recent controversy has raised the possibility that certain calcium antagonists are unsafe to use, especially for patients with coronary heart disease. Proarrhythmia has been proposed to be a mechanism contributing to potentially adverse outcomes. Although excessive concentrations of verapamil and diltiazem may cause sino-atrial nodal asystole and varying degrees of atrioventricular block, there is little direct evidence that this contributes to significant proarrhythmia, for example, ventricular tachyarrhythmias. Nonetheless, although it appears paradoxical that agents which block the entry of Ca2+ into heart cells may be considered arrhythmogenic, there are circumstances under which dosage with certain calcium antagonists potentially leads to myocardial Ca2+ overload. For example, bouts of neurohormonal activation brought about by calcium antagonist-induced abrupt reductions in blood pressure may be accompanied each time by significant beta-adrenergic-enhanced influx of Ca2+ through the L-type cardiac calcium channels. This elevates the intracellular Ca2+ concentration and disturbs Ca2+ regulation, especially in diseased hearts whose intracellular Ca2+ regulation has already been compromised, and might induce alterations in cardiac electrical activity. In the present article, interactions among cardiac calcium channels, classes of calcium antagonists, and specific formulations of certain antagonists are considered with respect to directly induced ventricular arrhythmogenesis. Indirect potentially proarrhythmic actions of the calcium antagonists are also discussed. We outline some of the many questions that remain to be answered with respect to the actions of DHP on the heart including that of whether beta-adrenergic stimulation modifies the degree of cardiac Ca2+ channel inhibition by DHP-type calcium antagonists.

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Multidrug resistance (MDR) presents a problem in cancer chemotherapy, and developing new agents to overcome MDR is important. This study intends to investigate the reversal effect of -elemene on MDR in human breast carcinoma MCF-7 and doxorubicin-resistant MCF-7 cells.

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Jejunal single-pass perfusion experiments with 120-mg/L (244 micromol/L) R-/S-verapamil were performed in 8 healthy male volunteers for 100 minutes before and after 14 days of oral treatment with St John's wort (300 mg 3 times a day). The enantiomers of verapamil and the cytochrome P450 (CYP) 3A4-formed metabolite norverapamil in perfusate and plasma were quantified by chiral HPLC with fluorescence and tandem mass spectrometry detection, respectively.

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Our results suggest that increasing HO-1 activity in hHeps protects them from oxidative stress-dependent damage. As polyphenols have great potential to induce HO-1 expression, they may play an important role for future therapeutic strategies to protect liver from oxidative stress-dependent damage observed during chronic alcohol consumption.

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Oxygen is essential for normal cardiac function and plays an important role in cardiac regulation. Electron paramagnetic resonance (EPR) oximetry appears to have some significant advantages for measuring oxygen tension (pO2) in the beating heart. This study presents the serial measurement of myocardial pO2 by EPR oximetry in the isolated crystalloid perfused heart during treatment with different cardioactive drugs: dobutamine, metoprolol, verapamil, vasopressin, and N omega-Nitro-L-Arginine Methyl Ester (L-NAME). Baseline myocardial pO2 was 176 +/- 14 mmHg (mean +/- S.E.). Myocardial capillary density in the intact contracting heart was calculated to be 2300 +/- 100 mm-2, using local myocardial pO2 and a cylindrical model for oxygen diffusion in tissue. Each drug had characteristic effects on myocardial pO2, myocardial oxygen consumption (MVO2), and capillary density. Metoprolol and verapamil increased myocardial pO2 by 51% and 18%, respectively, dobutamine decreased myocardial pO2 by 84% while vasopressin and L-NAME had no significant effect on myocardial pO2. Metoprolol and verpamil decreased MVO2 by 9% and 56%, respectively, while dobutamine increased MVO2 by 59%. A quantitative comparison of effects on the capillary bed based on changes in myocardial pO2 and MVO2 was made. Metoprolol and verapamil had opposite effects on the capillary bed. Verapamil decreased myocardial capillary density by 39%, while capillary density increased by 10% (n.s.) with metoprolol. Data following perfusion without drug is also presented. We conclude that: 1) The application of EPR oximetry with LiPc provides dynamic evaluation of local myocardial pO2 in the contracting heart. 2) Using a cylindrical model of oxygen delivery and diffusion in tissue, these data may be used to describe the changes of capillary density during pharmacological interventions.

calan eeze review

To investigate the dose-response relationship and contribution of verapamil SR and trandolapril given in combination once a day for the treatment of essential hypertension.

calan drug classification

Patients' (n=503) mean age was 84.4 years (range 80-102), and 61.2% was female. The median medication use was 5 (0-16). The mortality, hospitalisation, and institutionalisation rate were 8.9%, 31.0%, and 6.4% respectively. The mortality and hospitalisation group had a higher level of multimorbidity and weaker functional profile. Adjusted multivariate models showed an 11% increased hospitalisation rate for every additional medication taken. No association was found between high medication use and mortality, nor with institutionalisation. A higher association for mortality was observed among verapamil/diltiazem users, hospitalisation was higher among users of verapamil/diltiazem, loop diuretics and respiratory agents. Institutionalisation was higher among benzodiazepines users.

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AH-1058 is a newly synthesized antiarrhythmic agent. We investigated the antiarrhythmic and electrophysiological effects of AH-1058 in experimental arrhythmia models and isolated cardiomyocytes. In the ouabain-induced arrhythmia model of the guinea pig, pretreatment with AH-1058 (0.1-0.3 mg/kg, i.v.) delayed the appearance of premature ventricular complex (PVC) and ventricular fibrillation (VF) induced by intravenous infusion of ouabain. However, disopyramide (10 mg/kg, i.v.) delayed only that of PVC, and verapamil (1 mg/kg, i.v.) failed to affect the ouabain-induced ventricular arrhythmias. In the reperfusion-induced arrhythmia model of the rat, in which 5-min coronary occlusion and 10-min reperfusion were produced, AH-1058 (0.1-0.3 mg/kg, i.v.) inhibited the incidence of both ventricular tachycardia (VT) and VF, whereas disopyramide (5 mg/kg, i.v.) inhibited only reperfusion-induced VF. On the other hand, a higher dose of AH-1058 (1 mg/kg, i.v.) did not affect the aconitine-induced arrhythmias in rats, which were inhibited by disopyramide (5 mg/kg, i.v.). We also confirmed oral activity of AH-1058 in the reperfusion-induced arrhythmia model of the rat. AH-1058, at doses of 2-4 mg/kg, dose-dependently inhibited VT and VF. Electrophysiological experiments with patch-clamp techniques revealed that AH-1058 potently suppressed the L-type Ca2+ currents in isolated cardiomyocytes of the guinea pig. These results suggest that AH-1058 is a potent antiarrhythmic drug having a Ca2+ channel-blocking action. The antiarrhythmic profile of AH-1058 is different from that of disopyramide and verapamil.

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There is limited information on the effect of coronary artery vasodilators on coronary arterial distensibility.

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We examined the effect of different doses of calcium channel blockers on plasma cyclosporine levels. As previously reported by multiple investigators, we observed that the administration of verapamil or diltiazem, but not nifedipine or isradipine, caused a significant increase in plasma cyclosporine levels achieved for a given dose of cyclosporine. In this article, we show that the effect of verapamil and diltiazem on cyclosporine levels appears to be independent of dosage within their usual prescription range.

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Atrial flutter is a relatively rare but nonetheless important arrhythmia. Its mechanism and anatomy have been defined as right atrial macroreentry. It responds to treatment with a variety of antiarrhythmic agents but, in general, drug efficacy for acute termination is low. The addition of pacing to drug therapy markedly improves the success rate for restoration of sinus rhythm. Useful antiarrhythmic agents include amiodarone, sotalol, disopyramide, flecainide, and propafenone, but definitive efficacy studies have not been performed. The risk of provoking 1:1 AV conduction and a marked increase in ventricular response rate is always present. AV nodal blocking drugs (digoxin and verapamil) probably offer protection from this unwanted effect, but the prevalence of 1:1 conduction and the efficacy of AV nodal blockade remain to be established. When drug management fails, there is a place for radiofrequency ablation. Little is known about the thromboembolic risk of atrial flutter. As a consequence, the role of prophylactic anticoagulation is uncertain. Current interest in atrial flutter will ensure that these and other clinical questions are answered in the near future.

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Reactive oxidant species are implicated in the chronic airway inflammation related to asthma and chronic obstructive pulmonary disease. This study was designed to determine mechanisms underlying contraction induced by hydrogen peroxide (H(2)O(2)), a clinical marker of oxidative stress, in airway smooth muscle. Isometric tension and fluorescent intensities of fura-2, an index of intracellular Ca(2+) concentrations ([Ca(2+)](i)), were measured in epithelium-denuded tracheal smooth muscle tissues isolated from guinea pigs. H(2)O(2) (0.01-1 mM) caused contraction with an augmentation of [Ca(2+)](i) in a concentration-dependent manner in the normal physiological solution containing 2.4 mM of extracellular Ca(2+) concentrations. The contractile force and [Ca(2+)](i) by H(2)O(2) (1 mM) were approximately half of those in response to 1 microM methacholine. However, contraction by H(2)O(2) was not generated under the condition that extracellular Ca(2+) concentrations were less than 0.15 mM. Verapamil (10 microM), an inhibitor of voltage-operated Ca(2+) channels, partially but significantly inhibited the H(2)O(2)-induced contraction. In contrast, SKF-96365 (1-{beta-[3-(4-methoxyphenyl)propoxy]-4-methoxyphenethyl}-1H-imidazole hydrochloride) (100 microM), a non-selective inhibitor of Ca(2+) channels, completely abolished both the contraction and the increase in [Ca(2+)](i) elicited by H(2)O(2). Moreover, Y-27632 ((R)-(+)-trans-N-(4-Pyridyl)-4-(1-aminoethyl)-cyclohexanecarboxamide) (0.03-10 microM), an inhibitor of Rho-kinase, caused a concentration-dependent inhibition of the H(2)O(2)-induced contraction. In conclusion, both the Ca(2+) influx from the extracellular side and the Ca(2+) sensitization by Rho-kinase are involved in the regulation of airway smooth muscle tone induced by H(2)O(2). An inhibition of the Rho/Rho-kinase pathway may be beneficial for the treatment of airflow limitation mediated by oxidative stress.

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The microvascular distribution of oxygen was studied in the arterioles and venules of the awake hamster window chamber preparation to determine the contribution of vascular smooth muscle relaxation to oxygen consumption of the microvascular wall during verapamil-induced vasodilatation. Verapamil HCl delivered in a 0.1 mg/kg bolus injection followed by a continuous infusion of 0.01 mg.kg(-1).min(-1) caused significant arteriolar dilatation, increased microvascular flow and functional capillary density, and decreased arteriolar vessel wall transmural Po(2) difference. Verapamil caused tissue Po(2) to increase from 25.5 +/- 4.1 mmHg under control condition to 32.0 +/- 3.7 mmHg during verapamil treatment. Total oxygen released by the microcirculation to the tissue remained the same as at baseline. Maintenance of the same level of oxygen release to the tissue, increased tissue Po(2), and decreased wall oxygen concentration gradient are compatible if vasodilatation significantly lowers vessel wall oxygen consumption, which in this model appears to constitute an important oxygen-consuming compartment. These findings show that treatment with verapamil, which increases oxygen supply through vasodilatation, may further improve tissue oxygenation by lowering oxygen consumption of the microcirculation.

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This study describes the synergistic interaction of two calcium channel blockers, verapamil (VR) and SR33557 or fantofarone (SR), in reversing chloroquine resistance in Plasmodium falciparum, the causative agent of human malaria. The two calcium channel blockers exhibited an intrinsic antimalarial activity at 10 and 1 microM for verapamil and fantofarone, respectively. Isobolograms revealed that chloroquine and verapamil, and chloroquine and fantofarone, acted synergistically against chloroquine-resistant strains of P. falciparum. When used at subinhibitory concentrations, verapamil appeared 2 to 3 times more potent than fantofarone in reversing chloroquine resistance. Indeed, verapamil completely reversed the chloroquine resistance in P. falciparum, while fantofarone did so only partially. In the highly chloroquine-resistant strain FcB1, VR and SR acted synergistically to reverse CQ resistance, and the concentrations of VR used in these combinations could be reduced 10- or 100-fold (e.g. 100 nM and 10 nM) those required when this drug was used alone. In the moderately chloroquine-resistant strain K1, a combination of VR and SR for CQ resistance reversal allowed us to reduce the concentration of these chemosensitizers 1000- and 100-fold, respectively. The maximum tolerable plasma level beyond which side-effects occurred when using verapamil is 2.5 microM. Thus, the approach described, which allowed us to lower the doses of chemosensitizers, could well prevent toxic effects in humans and enlighten the advantages of polychemotherapy.

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It is difficult to accurately determine prognosis of patients with hypertension and chronic stable coronary artery disease (CAD). Our aim was to construct a risk score for predicting important adverse events in this population.

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It is known that calcium channel blockers induce Parkinsonism. In this study, amlodipine-, diltiazem-, and verapamil-induced catalepsy was investigated in mice. All of these three calcium channel blockers induced catalepsy. Dopamine D1, D2, and mACh receptor occupancies were estimated under the same conditions, and the affinities of these drugs for each receptor were also estimated in vitro. Intensity of catalepsy was predicted by dopamine D1, D2, and mACh receptor occupancies with the dynamic model which had already been constructed and was compared with the observed values. The predicted and the observed values were comparable (r = 0.98, p < 0.001). In conclusion, the dynamic model considering D1, and D2, and mACh receptor occupancy may be useful for quantitative prediction of drug-induced catalepsy.

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Randomized, open label, blinded end point study of 22 576 hypertensive CAD patients aged 50 years or older, which was conducted September 1997 to February 2003 at 862 sites in 14 countries.

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calan medication 2016-03-01

Silicon nanopowder (5-50 nm) was applied as a matrix for the analysis of small molecules in laser desorption/ionization mass spectrometry. In contrast with conventional matrix-assisted laser desorption/ionization (MALDI) time-of-flight mass spectrometry, the matrix background interference in the low mass range was significantly reduced. Effects of the particle size and sample preparation procedures on the background mass spectra and the analyte signal intensity have been investigated, and an optimized powder and sample preparation protocol was established. Several surface characterization tools have been applied as well. Both positive mode and negative mode laser desorption/ionization have been applied to different analytes including drugs, peptides, pesticides, acids, and others. Detection limits down to the low femtomole per microliter levels were achieved for propafenone and verapamil drugs. The method developed was found relatively tolerant to salt contamination, which allowed the direct analysis of morphine and propaphenone in untreated urine and triazine herbicides in a soil extract. The new silicon-nanoparticle-assisted laser desorption ionization method was found to be highly selective, which may be due to analyte-dependent precharging in solution, prior to vacuum laser desorption. Some aspects of the charge-transfer mechanism have been studied and discussed. In comparison with standard MALDI buy calan matrixes, the silicon nanopowder requires much lower laser fluence (contributing to a reduced background) has much better surface homogeneity, and is more tolerant to salt interference, which makes it an easily applicable practical tool at a potentially low cost.

calan eeze review 2016-02-02

A quasi-experimental prospective before and after study without a control group was conducted on 7289 patients diagnosed with hypertension who were on buy calan treatment with CRV, between October 1, 2012 and December 31, 2012 in 8 Colombian cities, collected from a database for dispensing medicines. Socio-demographic and pharmacological variables were evaluated. A total of 108 educational interventions were performed on those responsible for their health care, and evaluated within three months with the proportion of suspension of the prescriptions of CRV being evaluated. Multivariate analysis was performed using SPSS 22.0.

calan 40 mg 2017-10-03

In the mammalian heart, the circadian protein Clock regulates glucose and fatty acid metabolism. In this study, we determined some of the factors that regulate Clock expression and subcellular distribution in myocytes. Using immunochemistry and biochemical subcellular fractionation, we have shown that Clock localizes to the Z-disk of the myofilaments. Increasing calcium and cross-bridge cycling with 10 microM phenylephrine for 48 h resulted in a threefold increase in Clock and a translocation of the protein to the nucleus. When myofilament cross-bridge cycling was inhibited with 10 microM verapamil or 7.5mM butanedione monoxime for 48 h, both significantly reduced the presence of Clock buy calan in the nucleus and cytoskeleton. These results suggest that the expression and subcellular distribution of Clock can be altered by changes in cross-bridge cycling, a major source of energy expenditure in myocytes. We suggest that the circadian Clock protein may help coordinate the sensing of energy expenditure with energy supply.

calan drug classification 2016-01-02

To investigate the buy calan role of carrier mechanisms in: [1] the polarized transport of the bis(pivaloyloxymethyl)- [bis(POM)-] ester prodrug of the antiviral agent 9-(2-phosphonylmethoxyethyl)adenine [PMEA] and [2] the directional secretion of its metabolites.

calan 80 mg 2015-12-26

Salvia miltiorrhiza (SM buy calan , Danshen), a traditional Chinese herbal drug, has been widely used for hundreds of years to treat coronary artery disease.

calan 240 mg 2016-06-20

1. The present study was undertaken to analyse the mechanism of the contractile response induced by the bioflavonoid myricetin in isolated rat aortic rings. 2. Myricetin induced endothelium-dependent contractile responses (maximal value=21+/-2% of the response induced by 80 mM KCl and pD2=5.12+/-0 buy calan .03). This effect developed slowly, reached a peak within 6 min and then declined progressively. 3. Myricetin-induced contractions were almost abolished by the phospholipase A2 (PLA2) inhibitor, quinacrine (10 microM), the cyclo-oxygenase inhibitor, indomethacin (10 microM), the thromboxane synthase inhibitor, dazoxiben (100 microM), the putative thromboxane A2 (TXA2)/prostaglandin endoperoxide receptor antagonist, ifetroban (3 microM). These contractions were abolished in Ca2+-free medium but were not affected by the Ca2+ channel blocker verapamil (10 microM). 4. In cultured bovine endothelial cells (BAEC), myricetin (50 microM) produced an increase in cytosolic free calcium ([Ca2+]i) which peaked within 1 min and remained sustained for 6 min, as determined by the fluorescent probe fura 2. This rise in [Ca2+]i was abolished after removal of extracellular Ca2+ in the medium. 5. Myricetin (50 microM) significantly increased TXB2 production both in aortic rings with and without endothelium and in BAEC. These increases were abolished both by Ca2+-free media and by indomethacin. 6. Taken together, these results suggests that myricetin stimulates Ca2+ influx and subsequently triggers the activation of the PLA2 and cyclo-oxygenase pathways releasing TXA2 from the endothelium to contract rat aortic rings. The latter response occurs via the activation of Tp receptors on vascular smooth muscle cells.

calan 180 mg 2017-10-09

Erythroxylum caatingae Plowman has a myorelaxing effect on smooth muscle tissue. We investigated the effect of the crude ethanolic extract of E. caatingae Plowman (Ec-EtOH) on the contractility of the ovine cervix. In an isometric system, circular strips were subjected to 90mM potassium (K(+)) or 30μM carbamylcholine (CCh)-induced contraction. We then exposed the tissue to cumulative concentrations of Ec-EtOH (1-729 μg/ml). In other bath solutions, the tissues were exposed to l-NG-nitroarginine methyl ester (l-NAME; 100μM), l-NAME (100μM)+l-arginine (300μM), 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, ODQ; 5μM), 4-aminopyridine (4-AP; 3mM), tetraethylammonium (TEA; 0.3mM), glybenclamide (1μM), atosiban (10μM) or verapamil (3μM), followed by the addition of Ec-EtOH (1-729 μg/ml). We also buy calan evaluated the effect of cervical Ec-EtOH infusion (2mg) on cervical contractility in vivo. Ec-EtOH decreased cervical contractility induced by K(+) or CCh, and 729 μg/ml Ec-EtOH decreased 85.4±5.1% the amplitude of basal contractility in vitro, with an EC50 of 17.9±3.7 μg/ml. This effect of Ec-EtOH was prevented by l-NAME or ODQ. l-arginine impaired the blunting effect of l-NAME on cervical relaxation caused by Ec-EtOH. However, the potassium channel blockers 4-AP, TEA, and glybenclamide did not modify this myorelaxation triggered by Ec-EtOH. Ec-EtOH also decreased acetylcholine-induced contractions in tissue preincubated with verapamil. In addition, Ec-EtOH decreased ovine cervical contractions in vivo. Thus, Ec-EtOH had a relaxant effect on ovine cervical contractions. This may involve the nitric oxide signal, mediated by cGMP cellular transduction, and be related to intracellular calcium sequestration.

calan drug 2017-11-13

Circular muscle strips (2.0 x 0.2 cm) were buy calan prepared from the corpus of cat stomach in order to measure isometric contraction in a chamber filled with Krebs-Ringer solution (pH 7.4, temperature 36 degrees C) bubbled with 5% CO2 in O2.

calan reviews 2015-04-09

Although LCM is a substrate of Pgp in CETA, Caco-2 data demonstrated that passive diffusion should play a major role in the overall disposition of LCM. buy calan The critical role of Pgp should be addressed in vivo.

calan tablets 2016-05-09

In the context of pharmaceutical development today, studies for pediatric drug approval are requested more and more often by the regulatory authorities. The developing lung represents a potential target in juvenile toxicity studies. Due to physiological differences in prenatal and postnatal development between humans and standard animal models, experimental methods have to be modified to assess pulmonary function, and basic data on respiratory parameters need to be provided. Daily nose-only inhalation exposure from postnatal days 4 to 21 using a model substance (verapamil HCl) and plethysmographic measurements between postnatal days 2 and 50 were performed noninvasively in conscious juvenile Wistar (WU) rats. The methods proved to be feasible and did buy calan not interfere with normal growth and development of the animals. Both techniques therefore permit new insights to support human neonatal risk assessment and therefore these animal models are suitable for regulatory studies.

calan dosage 2016-05-18

Midazolam and diazepam have differential effects on cardiac E-C coupling. Diazepam, but buy calan not midazolam, enhances cardiac E-C coupling independent of L-type Ca2+ channel modulation.

calan pill 2016-11-20

The purpose of this study was to identify conditions that will increase the sensitivity of resistant cancer cells to anti-mitotic drugs. Currently, atovaquine (ATO), chloroquine (CHL), primaquine (PRI), mefloquine (MEF), artesunate (ART), and doxycycline (DOY) are the most commonly used anti-malarial drugs. Herein, we tested whether anti-malarial drugs can sensitize drug-resistant KBV20C cancer cells. None of the six tested anti-malarial drugs was found to better sensitize the drug-resistant cells compared to the sensitive KB cells. With an exception of DOY, all other anti-malarial drugs tested could sensitize both KB and KBV20C cells to a similar extent, suggesting that anti-malarial drugs could be used for sensitive as well as resistant cancer cells. Furthermore, we examined the effects of anti-malarial drugs in combination with an antimitotic drug, vinblastine (VIN) on the sensitisation of resistant KBV20C cells. Using viability assay, microscopic buy calan observation, assessment of cleaved PARP, and Hoechst staining, we identified that two anti-malarial drugs, PRI and MEF, highly sensitized KBV20C-resistant cells to VIN treatment. Moreover, PRI- or MEF-induced sensitisation was not observed in VIN-treated sensitive KB parent cells, suggesting that the observed effect is specific to resistant cancer cells. We demonstrated that the PRI and MEF sensitisation mechanism mainly depends on the inhibition of p-glycoprotein (P-gp). Our findings may contribute to the development of anti-malarial drug-based combination therapies for patients resistant to anti-mitotic drugs.

calan 120 mg 2016-03-30

Microelectrode array (MEA) approaches have been proposed as a tool for detecting functional changes in electrically excitable cells, including neurons, exposed to drugs, chemicals or particles. However, conventional single well-MEA systems lack the throughput necessary for screening large numbers of uncharacterized compounds. Recently, multi-well MEA (mwMEA) formats have become available to address the need for increased throughput. The current experiments examined the effects of a training set of 30 chemicals on spontaneous activity in networks of cortical neurons grown on mwMEA plates. Each plate contained 12 wells with 64 microelectrodes/well, for a total of 768 channels. Of the 30 chemicals evaluated, 23 were known to alter neuronal function in vivo ("positives"), including 6 GABAergic and 3 glutamatergic antagonists/agonists, 4 buy calan pyrethroids, 3 metals, 2 cholinesterase inhibitors, 2 nicotinic acetylcholine receptor agonists, valproic acid, verapamil, and fluoxetine. Seven compounds expected to have no effect on neuronal function were tested as "negatives" (glyphosate, acetaminophen, salicylic acid, paraquat, saccharin, d-sorbitol and amoxicillin). Following collection of 33 min of baseline activity, chemical effects (50 μM or highest soluble concentration) were recorded for 33 min. Twenty of the positives altered the mean network spike rate by more than the 14% threshold (two standard deviations from the mean for DMSO control). The three positives without effect were bifenthrin, nicotine and imidacloprid. None of the negative compounds caused a change in activity beyond the threshold. Based on these results, the mwMEA assay has both high sensitivity (87% identification of positive compounds) and specificity (100% identification of negative compounds). These experiments demonstrate the capacity of mwMEAs to screen compounds for neurotoxic effects mediated by a broad variety of mechanisms.

calan sr dosage 2015-11-27

Achillea millefolium Linn. (Asteraceae) is used in folk medicine for the treatment of overactive cardiovascular and respiratory ailments. This study describes its hypotensive, cardio-depressant, vasodilatory and bronchodilatory activities. The crude extract of Achillea millefolium (Am.Cr) caused a dose-dependent (1-100 mg/kg) fall in arterial blood pressure of rats under anaesthesia. In spontaneously beating guinea-pig atrial tissues, Am.Cr exhibited negative inotropic and chronotropic effects. In isolated rabbit Zocor Dosage Elderly aortic rings, Am.Cr at 0.3-10 mg/mL relaxed phenylephrine (PE, 1 µm) and high K(+) (80 mm)-induced contractions, as well as suppressed the PE (1 µm) control peaks obtained in Ca(++) -free medium, like that caused by verapamil. The vasodilator effect of Am.Cr was partially blocked by N(ω) -nitro-l-arginine methyl ester in endothelium intact preparations. In guinea-pig tracheal strips, Am.Cr inhibited carbachol (CCh, 1 µm) and K(+) -induced contractions. These results indicate that Achillea millefolium exhibits hypotensive, cardiovascular inhibitory and bronchodilatory effects, thus explaining its medicinal use in hyperactive cardiovascular and airway disorders, such as hypertension and asthma.

calan dosage forms 2015-01-29

Inhibition of BCL2 proteins is one of the most promising new approaches to targeted cancer therapy resulting in the induction of apoptosis. Amongst the most specific BCL2-inhibitors identified are ABT-737 and ABT-263. However, targeted therapy is often only effective for a limited amount of time because of Norvasc Tablet Uses the occurrence of drug resistance. In this study, the interaction of BCL2-inhibitors with the drug efflux transporter P-glycoprotein was investigated. Using (3)H labelled ABT-263, we found that cells with high P-glycoprotein activity accumulated less drug. In addition, cells with increased P-glycoprotein expression were more resistant to apoptosis induced by either ABT-737 or ABT-263. Addition of tariquidar or verapamil sensitized the cells to BCL2-inhibitor treatment, resulting in higher apoptosis. Our data suggest that the BCL2-inhibitors ABT-737 and ABT-263 are substrates for P-glycoprotein. Over-expression of P-glycoprotein may be, at least partly, responsible for resistance to these BCL2-inhibitors.

calan generic name 2015-11-23

P-Glycoprotein, a 170-180 kDa membrane glycoprotein that mediates multidrug resistance, hydrolyses ATP to efflux a broad spectrum of hydrophobic agents. To observe the interaction of a P-gp reversal agent with P-gp ATPase activity should provide further insights Prilosec 75 Mg into the mechanisms of P-gp modulator. In this study, we analysed the effect of CJZ3, a lomerizine derivative, on the adenosine triphosphatase (ATPase) activity of human P-glycoprotein. The results showed that the basal P-gp ATPase activity was increased by CJZ3 with half-maximal activity concentration (Km) of 6.8 +/- 1.5 microM, CJZ3 may interact with P-gp with a higher affinity and exhibit a more potent effect than verapamil (Ver). Kinetic analysis indicated a noncompetitive inhibition of Ver-stimulated P-gp ATPase activity and a competitive inhibition of CJX2-stimulated P-gp ATPase activity by CJZ3, moreover, the effect of CsA on CJZ3-stimulated and Ver-stimulated P-gp ATPase activity showed a non-competitive and a competitive inhibition respectively. CJZ3 and CJX2 can bind P-gp either on overlapping sites or distinct but interacting sites, while CJZ3 and Ver as well as CsA can bind P-gp on separated sites in K562/DOX cells.

calan overdose 2017-05-03

The mechanisms of UTP-induced contractions in the rat aorta strips were studied. These were only partially inhibited in a Ca(2+)-free medium or by incubation with verapamil or nifedipine. Successive challenges did not decrease the magnitude of the contraction in the absence of external Ca(2+). Quin 2(acetoxymethyl) ester (Quin 2AM), 8-(N,N-diethylamino)octyl 3,4,5-trimetoxybenzoate (TMB-8), thapsigargin and ryanodine inhibited these contractions. The participation of protein kinase C is also very likely, since downregulation by the phorbol 12,13 dibutyrate (PDB) decreased UTP-induced contraction, and staurosporine and 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7) antagonized UTP-induced contractions and relaxed UTP-induced tonic contractions. Therefore, different pools of intracellular Ca(2+) and protein kinase C seem to participate in UTP-induced contraction and in the mechanisms of maintenance in a Famvir Medicine Ca(2+)-free medium.

calan sr medication 2017-05-06

Use of advanced imaging (CT/MRI), opioids/barbiturates, Arcoxia With Alcohol and referrals to other physicians (guideline-discordant indicators), as well as counseling on lifestyle modifications and use of preventive medications including verapamil, topiramate, amitriptyline, or propranolol (guideline-concordant during study period). We analyzed results using logistic regression, adjusting for patient and clinician characteristics, and weighted to reflect U.S. population estimates. Additionally, we stratified findings based on migraine versus non-migraine, acute versus chronic symptoms, and whether the clinician self-identified as the primary care physician.

calan 5 mg 2016-08-16

Fluoxetine (FLX), a P-glycoprotein inhibitor with antimalarial activity, is promising candidate for reversing chloroquine/mefloquine (CQ/MQ) resistance. The Dd2 strain of CQ- and MQ-resistant Plasmodium falciparum was synchronized and assayed with various concentrations of CQ/MQ individually and in combination with FLX or verapamil (VPL). Our results indicated the 50% inhibitory concentration values of CQ and MQ were greatly lowered when FLX was used simultaneously. Isobolograms indicated that CQ-FLX combinations are more synergistic (mean fractional inhibitory concentration [FIC] index 0.55) than MQ-FLX (mean FIC index 0.64), and their Cleocin Name Brand synergistic effect was better than or at par with CQ-VPL (mean FIC index 0.88) and MQ-VPL (mean FIC index 0.60) combinations. We conclude that the FLX potentiates the CQ and MQ response on multidrug-resistant P. falciparum at clinically achievable concentrations.

calan tab 2016-05-14

Hydrogen-3-daunomycin cellular accumulation was never modified by more than 15% when compared Prevacid Recommended Dosage to control values, while 99mTc-sestamibi decreased to 75% +/- 32% (m +/- s.d.) of controls in the presence of S9788 and to 44% +/- 19% when S9788 was associated with verapamil.