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Calan (Verapamil Hydrochloride)

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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:
Bosoptin, Calan, Calaptin, Covera-HS, Isoptin, Isoptin SR, Verelan, Verelan PM, VPL, Zolvera

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Cartia XT, Cardizem, Cardizem LA, Nifedical XL , Propranolol, Procardia, Procardia XL

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Also known as:  Verapamil Hydrochloride.


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.


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.


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.


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.


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 120 mg

The role of Ca2+-activated K+-channel, ATP-sensitive K+-channel, and delayed rectifier K+-channel modulation in the canine pulmonary vascular response to hypoxia was determined in the isolated blood-perfused dog lung. Pulmonary vascular resistances and compliances were measured with vascular occlusion techniques. Under normoxia, the Ca2+-activated K+-channel blocker tetraethylammonium (1 mM), the ATP-sensitive K+-channel inhibitor glibenclamide (10(-5) M), and the delayed rectifier K+-channel blocker 4-aminopyridine (10(-4) M) elicited a small but significant increase in pulmonary arterial pressure. Hypoxia significantly increased pulmonary arterial and venous resistances and pulmonary capillary pressure and decreased total vascular compliance by decreasing both microvascular and large-vessel compliances. Tetraethylammonium, glibenclamide, and 4-aminopyridine potentiated the response to hypoxia on the arterial segments but not on the venous segments and also further decreased pulmonary vascular compliance. In contrast, the ATP-sensitive K+-channel opener cromakalim and the L-type voltage-dependent Ca2+-channel blocker verapamil (10(-5) M) inhibited the vasoconstrictor effect of hypoxia on both the arterial and venous vessels. These results indicate that closure of the Ca2+-activated K+ channels, ATP-sensitive K+ channels, and delayed rectifier K+ channels potentiate the canine pulmonary arterial response under hypoxic conditions and that L-type voltage-dependent Ca2+ channels modulate hypoxic vasoconstriction. Therefore, the possibility exists that K+-channel inhibition is a key event that links hypoxia to pulmonary vasoconstriction by eliciting membrane depolarization and subsequent Ca2+-channel activation, leading to Ca2+ influx.

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The role of extracellular Ca2+ in the maintenance of chronic vasospasm after subarachnoid hemorrhage (SAH) is largely unknown. Indeed, studies thus far have been limited to demonstrations that L-type Ca(2+)-channel antagonists were unable to reverse the spasm. This study tested whether SAH-induced vasospasm is maintained, at least in part. through the influx of extracellular Ca2+ and whether the influx of extracellular Ca2+ occurs through L-type Ca2+ channels and possibly, in addition, through store operated channels (SOCs). Furthermore, as there is considerable evidence in the literature to suggest that the spasm is mediated through endothelin-1 (ET-1) release, we tested whether the Ca2+ dependency of the spasm was consistent with the mediation of the spasm by ET-1.

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We report a common HPLC method for the single or simultaneous determination of four calcium channel blockers (CCB), namely diltiazem (DTZ), verapamil (VER), nifedipine (NIF) and nitrendipine (NIT) and their active metabolites demetildiltiazem and deacetildiltiazem (MA and M1), norverapamil (NOR), and dehydronifedipine (DHN). DHN was first synthesised in our laboratory and different pH values of the mobil phase were subsequently prepared and tested for chromatographic separation. The detection system and the environmental light conditions were optimised. The best separations of all analytes were obtained using a C(18) column and a mobile phase of methanol, 0.04 M ammonium acetate, acetonitrile and triethylamine (2:2:1:0.04 v/v). Quantitation was performed using imipramine (IMI) as the internal standard. For DTZ and its metabolites (M1 and MA), the wavelength chosen was 237 nm; for VER and its metabolite NOR, it was 210 nm; and, finally for NIF and its metabolite DHN and NIT it was 216 nm. When a simultaneous analysis was carried out the wavelength was of 230 nm. The optimum pH were 7.90 and 7.10 when the separation of NIT and DTZ or VER and NIF were carried out, respectively, and 7.90 when a simultaneous separation was carried out. The detection limit of the assay was less than 8 ng ml(-1) for all compounds, with coefficients of variation less than 7% (for inter- and intra-day) over the concentration range of 1-1000 ng ml(-1). The retention times were less than 11 min. When NIF or NIT were studied, it was necessary to use a sodium vapour lamp in order to avoid the photodegradation which takes place under daylight conditions.

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Our findings provide some evidence for a role of tissue PhS in the tissue distribution of basic drugs with respect to stereoselectivity of drug enantiomers distribution.

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Calcium channel blocker (CCB) toxicity, in particular that induced by verapamil and diltiazem, presents clinical challenges with no true antidote. Levosimendan, a calcium sensitizer, improves cardiac contractility in patients with heart failure. We tested the hypothesis that calcium channel sensitization will prolong survival in a rat model of severe verapamil poisoning.

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Administration of drugs by inhalation opens new possibilities for entry into the systemic circulation and cultures of porcine pulmonary epithelial cells (PECs) may prove to be valuable in the prediction of pulmonary metabolism of drugs in humans. This paper, therefore, reports a method for the routine isolation and cultivation of PECs from slaughterhouse animals. On average 1.5x10(6) cells g-1 tissue were isolated by discontinuous density-gradient centrifugation. Cells were subsequently cultivated on collagen-coated plates and characterized by staining for alkaline phosphatase, by tannic acid staining of lamellar bodies and by surfactant protein (SP) expression at days 0, 3 and 6 in culture. Over 70% of purified cells were positive for SP-C and tannic acid staining and thus defined as epithelial cells of alveolar origin (AECs). The AEC phenotype was also confirmed by specific binding of marker lectins (Maclura pomifera and Helix pomatia) and by studying gene expression and activity of cytochrome P450 monooxygenases. Testosterone, ethoxyresorufin, benzyloxyresorufin and verapamil were used as substrates for cytochrome P450-catalysed oxidations and cultured cells were found to be differentiated as well as metabolically competent during cultivation. Therefore, this culture system enables in depth pulmonary biotransformation and toxicity studies.

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Pretreatment with verapamil alone does not improve maintenance of sinus rhythm after DC cardioversion in patients with AF. The rate of spontaneous cardioversion may be improved by verapamil.

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Profound renal vasoconstriction in UUO was associated with an increase in renal production of ET-1, possibly contributing to renal vasoconstriction, and was reversed by intrarenal infusion of verapamil.

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Purpose/Aim of the study: The purpose of this study was to evaluate the interaction between Polycystic ovary syndrome (PCOS) and Meibomian gland dysfunction (MGD) and obesity, to reveal whether there is a correlation between the testosterone levels and body-mass index (BMI) levels and the dry-eye complaints of these patients.

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Sevoflurane appears to block chorionic arterial KCa++ and KATP channels. Sevoflurane also blocks voltage-operated calcium channels, and exerts a net vasodilatory effect in the in vitro foeto-placental circulation.

calan 80 mg

Twenty patients with neuroblastoma who have been treated in our hospital since January 2005 were divided into pre-operative chemotherapy (10 patients) and non-chemotherapy (10) groups. Tumor specimens of the patients were taken and paraffin sections were made. The expressions of stem cell markers CD133, ABCG2, CD117 and nestin were immunohistochemically detected in the specimens. Neuroblastoma cells were stained with Hoechst 33342 and PI. The side population (SP) cells were analyzed by the fluorescence-activated cell sorter. The disparity drug resistance to cisplatin (DDP) of SP and non-SP cells was measured with MTT colorimetric assay. The oncogenicity of SP and non-SP cells was identified in nude mice.

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1. Cytosolic calcium concentration ([Ca2+]i) by indo 1 microspectrofluorimetry in freshly isolated cells and isometric contraction of isolated rings were measured in response to muscarinic cholinoceptor stimulation in rat tracheal smooth muscle. 2. In isolated myocytes, acetylcholine (ACh, 0.03-1 microM) caused a rapid and graded increase in [Ca2+]i up to a net amplitude of 492 +/- 26 nM (n = 19) which gradually declined. The EC50 for ACh was 0.13 microM. This first [Ca2+]i peak was followed, when the ACh concentration increased, in approximately 50-60% of the cells, by successive peaks of decreased amplitude ([Ca2+]i oscillations) superimposed on the plateau phase. Whereas the percentage of cells exhibiting [Ca2+]i oscillations remained consistent, the frequency of these oscillations increased to up to 10 min-1 with an ACh concentration of 100 microM. 3. Removal of extracellular calcium (in the presence of EGTA, 0.4 mM) or addition of the voltage-dependent Ca(2+)-channel blocker verapamil (10 microM) did not alter the first [Ca2+]i peak, the plateau or the oscillations induced by ACh or carbachol. In contrast, the specific inhibitor of the sarcoplasmic Ca(2+)-ATPase, thapsigargin (1 microM), completely abolished the [Ca2+]i response. Thapsigargin (1 microM) also blocked the caffeine (5 mM)-induced transient rise in [Ca2+]i. 4. Atropine (a non-selective muscarinic cholinoceptor antagonist) and 4-diphenyl acetoxy N-methyl piperidine (4-DAMP, a selective M3 antagonist) inhibited the [Ca2+]i response to muscarinic cholinoceptor activation with an IC50 of 13 and 20 nM, respectively. Pirenzepine (a selective M1 antagonist) also totally inhibited the [Ca2+]i response to ACh but with a higher IC50 of 2 microM. Methoctramine (a selective M2 antagonist) up to a concentration of 10 microM caused only a 40% inhibition. The effect of muscarinic antagonists on cumulative concentration-response curves (CCRC) for carbachol was assessed at the following concentrations: atropine and 4-DAMP at 3, 10 and 30 nM; pirenzepine 0.3, 1 and 3 microM, and methoctramine at 1, 3 and 10 microM. For these concentrations, all of the antagonists produced a rightward shift of the CCRC for carbachol and pA2 values were 9.2, 8.8, 6.7 and 6.3, respectively. 5. In conclusion, the present study indicates that muscarinic stimulation of rat isolated tracheal smooth muscle cells induces [Ca2+]i oscillations. The occurrence of these oscillations depends on the graded amplitude of the first [Ca2+]i rise and their frequency may play a role in the amplitude of the mechanical activity in response to muscarinic cholinoceptor activation. Both the [Ca2+]i and the contractile responses are primarily dependent on activation of the M3 receptor subtype.

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calan 80 mg 2015-03-15

Patients in the 2 groups were balanced in terms of baseline Zofran 2mg Dosage characteristics. In the heparin group, activated partial thromboplastin times were normal to mildly elevated; no clinically significant hemorrhages or instances of heparin-induced thrombocytopenia or deep vein thrombosis were encountered. In the control group, the incidence of clinical vasospasm requiring rescue therapy (induced hypertension, selective intraarterial verapamil, and angioplasty) was 20 (47%) of 43 patients, and 9 (21%) of 43 patients experienced a delayed infarct on CT scanning. In the heparin group, the incidence of clinical vasospasm requiring rescue therapy was 9% (4 of 43, p = 0.0002), and no patient suffered a delayed infarct (p = 0.003).

calan 240 mg 2015-06-02

Despite the availability of many newer antihypertensive agents, hypertensive patients remain at a higher risk of premature death than the general population. This persistence of elevated morbidity and mortality may be accounted for by the frequent failure to achieve adequate blood pressure reduction despite an extensive range of available antihypertensive agents. Such considerations have led to the reassessment of the potential role of fixed-dose combination agents. The antihypertensive efficacy may be enhanced when two classes of agents are combined. In addition, combination therapy enhances tolerability because one drug of fixed combination can antagonize some of the adverse effects of the second drug. Fixed-dose combination therapy simplifies the Desyrel And Alcohol treatment regimen, preventing treatment failures that might result from missed doses.

calan pill 2017-05-24

The effect of clomiphene, an ovulation-inducing agent, on cytosolic free Ca2+ levels ([Ca2+]i) in populations of BFTC human bladder cancer cells Paxil Replacement Drugs was explored by using fura-2 as a Ca2+ indicator.

calan eeze review 2015-05-19

The present method can readily be used to screen new-compound transport by P-gp or BCRP, even before any radiolabeling. Compounds that were previously thought to be transported by P-gp in rodents, such as p-MPPF, WAY-100635, and flumazenil, cannot be considered substrates of human P-gp. The impact of BCRP and P-gp at the BBB on the transport of befloxatone and diprenorphine in vivo remains Asacol Drug Class to be evaluated with PET.

calan tab 2017-06-01

A series of dihydrobenzopyrans and tetrahydroquinolines was synthesized and pharmacologically tested for their ability to inhibit P-glycoprotein mediated Diflucan Single Dose daunomycin efflux in multidrug resistant CCRF-CEM vcr1000 cells. Several compounds exhibit activities in the range of the reference compounds verapamil and propafenone. Preliminary structure-activity relationship studies propose the importance of high molar refractivity values of the compounds and the presence of an additional basic nitrogen atom.

calan 180 mg 2015-04-24

The multidrug resistant cell line CEM/VBL300 and the parental CEM T-lymphoblastic cell line from which it was derived were used to study the accumulation of fluorescent phospholipid analogs of phosphatidylcholine (PC), phosphatidylethanolamine (PE), and phosphatidylserine (PS). The fluorescent analogs NBD-PC, NBD-PE, and NBD-PS and [3H]PC were delivered in liposomes prepared by ethanol injection. Fluorescence microscopy demonstrated decreased accumulation of the NBD-PC analog in the multidrug resistant cell line compared to the parental cell line. Verapamil enhanced NBD-PC accumulation in the resistant cells. Similar results were obtained with insect cells expressing high levels of recombinant human MDR1. Prograf Missed Dose Elimination of NBD fluorescence on the outer leaflet of the plasma membrane with dithionite permitted quantification of the internal cellular fluorescence by FACS analysis. The drug resistant CEM/VBL300 cells accumulated approximately 10% the amount of NBD-PE and 20% the amount of NBD-PC compared to CEM drug sensitive cells. No difference in internal accumulation of NBD-PS was found between the drug resistant and drug sensitive cell lines. The internal accumulation of NBD-PE and NBD-PC was enhanced by the MDR reversal agents verapamil, cyclosporin A, and SDZ PSC 833 in the CEM/VBL300 cells but not in the CEM cells. The increased accumulation was dose dependent, and the relative potency of the reversal agents paralleled their ability to circumvent multidrug resistance. In addition, the monoclonal antibody UIC2 directed against the P-glycoprotein produced similar results. The evidence presented here suggests that PC and PE but not PS behave as substrates for human MDR1 P-glycoprotein.

calan 120 mg 2016-05-22

The intestinal absorptive characteristics of imperialine are closely related Augmentin Xr Generic to its physicochemical properties. The passive membrane diffusion dominates the intestinal absorption of imperialine.

calan generic name 2015-07-11

Homeostasis imbalance of intracellular Ca(2+) is one of the key pathophysiological factors in skeletal muscle injuries. Such imbalance can cause significant change Cost Sporanox Australia in the metabolism of Ca(2+)-related biomarkers in skeletal muscle, such as superoxide dismutase (SOD), malondialdehyde (MDA) and creatine kinase (CK). Measurements of these biomarkers can be used to evaluate the degree of damage to human skeletal muscle cells (HSKMCs) injury. Rolling manipulation is the most popular myofascial release technique in Traditional Chinese Medicine. The mechanism of how this technique works in ameliorating muscle injury is unknown. This study aimed to investigate the possible Ca(2+) mediated effects of intermittent pressure imitating rolling manipulation (IPIRM) of Traditional Chinese Medicine in the injured HSKMCs.

calan sr dosage 2016-06-11

P-glycoprotein (P-gp) is a drug efflux pump expressed Glucotrol 50 Mg , amongst others, on the luminal surface of the cerebral endothelial cells forming the blood-brain barrier. Studies in rodents have demonstrated that antihistamines that are substrates of the P-gp transporter display no or minor central nervous system (CNS) effects as compared to antihistamines that are not P-gp transporter substrates.

calan medication 2016-07-25

The CONVINCE trial did not demonstrate equivalence of a COER verapamil-based antihypertensive regimen compared with a regimen beginning with a diuretic or beta-blocker. When considered in the context of other trials of calcium antagonists, these data indicate that the effectiveness of calcium-channel therapy in reducing Alesse Review cardiovascular disease is similar but not better than diuretic or beta-blocker treatment.

calan 40 mg 2015-02-01

The aim of the study was to report a concentration-dependently biphasic effect of verapamil (VER) on the transport of phenobarbital (PB) across the blood-brain barrier (BBB) in vitro and in vivo. The uptake of PB by rat brain microvessel endothelial cells (rBMECs) and transport of PB across the rBMEC monolayer from apical to basolateral and basolateral to apical were evaluated in the presence of VER. The effect of VER on PB pharmacological activity on the central nervous system (CNS) and brain distribution of PB in mice were further investigated. The results showed that VER regulated the uptake of PB by rBMECs in a concentration-dependently biphasic manner. The uptake of PB by rBMECs was decreased by low concentrations of VER (1-25 μΜ), but increased by high concentrations of VER (50-300 μM). The biphasic regulation was also observed in transport experiment. In vivo studies showed that VER altered the pharmacological effect of PB on CNS and brain concentration of PB in a biphasic manner. In contrast to low doses of VER (0.125-0.5 mg/kg) that shortened the duration time of PB-induced loss of the righting reflex, high doses of VER (2-4 mg/kg) prolonged the duration time. Further study demonstrated that brain concentration of PB was decreased by 0.125 mg/kg VER, but increased by 2 mg/kg VER. The concentration-dependently biphasic regulation was also confirmed in the uptake of rhodamine 123 by rBMECs. Our results suggested that VER may regulate the transport of PB across BBB in a concentration-dependently biphasic manner and the biphasic regulation may be involved in P-gp function.