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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.

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These data indicate that applying transdermal verapamil gel to the penile shaft results in a small amount of systemic absorption but the gel does not infiltrate the tunica albuginea. Based on these findings the use of transdermal verapamil for Peyronie's disease has no scientific basis.

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Verapamil was instituted, resulting in prompt and sustained resolution of symptoms.

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Syl611 is an effective and potential agent in reversing multidrug resistance (MDR) by multiple actions, which attributed to p-glycoprotein inhibition and drug permeability enhancement.

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Rhodamine (Rh123) efflux was used to study ABCB1 activity, with or without the addition of the ABCB1 inhibitor verapamil. Intracellular interleukin (IL) 2 production in T cells was used to measure the pharmacodynamic effect of tacrolimus after phorbol-12-myristate-13-acetate/ionomycin stimulation of whole blood. In addition, the ABCB1 genotype of 36 tacrolimus-treated renal transplant patients was related to ABCB1 activity and tacrolimus efficacy.

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Ca2+ plays an essential role in pituitary adenylate cyclase-activating polypeptide (PACAP)-stimulated growth hormone (GH) secretion from porcine somatotropes. Here, Indo-1 microfluorimetry was used to investigate the dynamics of free cytosolic Ca2+ concentration ([Ca2+]i) in single porcine somatotropes in response to PACAP38 and PACAP27. We also evaluated the relative contributions of extra- and intracellular Ca2+ sources and of cAMP-dependent protein kinase (PKA) and phospholipase C (PLC). A high proportion of somatotropes responded to PACAP38 (79.4%) and PACAP27 (68.4%) with [Ca2+]i rises that could be followed by a refractory plateau (type 1 response), or by a decrease in [Ca2+]i during which somatotropes were responsive to a subsequent PACAP pulse (type II response). Although Ca2+ profiles in response to both peptides were similar, PACAP38-induced [Ca2+]i rises were higher. Somatotrope response to PACAP38 or PACAP27 was markedly reduced by removing extracellular Ca2+, blocking Ca2+ entry through L-type voltage sensitive Ca2+ channels (VSCC), or inhibiting PKA. Conversely, Ca2+ depletion from intracellular stores or PLC inactivation did not affect the response to PACAP27 but considerably reduced maximal [Ca2+]i induced by PACAP38. We conclude that both peptides stimulate extracellular Ca2+ influx through L-type VSCC by a PKA-dependent mechanism. However, PACAP38 also triggers a PLC-mediated Ca2+ mobilization from intracellular stores, thereby indicating that the two molecular forms of PACAP activate common and distinct second messenger pathways within porcine somatotropes.

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The right cervical vagal nerve was stimulated in five dogs. In one dog, right thoracotomy was performed to isolate the vagal nerve. Bipolar hook electrodes were attached to the vagal nerve. The vagal nerve was stimulated (3-5 mA, 40 Hz) for a few seconds while suturing the coronary artery. Experiments were conducted in two groups. In Group I, two dogs received vagal stimulation via the right neck, and one dog received vagal stimulation via the right thoracic cavity approach. In Group H, all vagal stimulations were performed via the neck during intravenous infusion of diltiazem (10 mg/hrs) or verapamil (5 mg/hrs).

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The objective of this work was to assess, in vitro, the passage of P-glycoprotein dependent drugs across brain capillary endothelial cells, when these drugs are associated with a reversing agent.

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The present study investigated the mechanisms of melatonin-induced inhibition of the ileal smooth muscle contraction. Rat isolated ileal smooth muscle strips were stimulated in an organ bath using carbachol (CAR) or potassium chloride (KCl) depolarization. Under these conditions, melatonin produced a concentration-dependent inhibition of muscle contraction (mean inhibitory concentration, IC50: 17.3 x 10(-6) M), which was not blocked by either tetrodotoxin (10(-6) M), hexamethonium (10(-4) M), or phentolamine (10(-6) M). The inhibitory effect of melatonin during CAR stimulation was blocked in a concentration-dependent manner by the presence of apamin (4.8 x 10(-9) M), a K(+)-channel blocker. By contrast, other K(+)-channel blockers such as 4-aminopyridine (10(-4) M to 5 x 10(-3) M), tetraethylammonium (10(-4) to 10(-1) M), and glibenclamide (10(-5) M) were ineffective. Additionally, the Ca(2+)-channel antagonists nitrendipine (IC50: 2.4 x 10(-9) M) and verapamil (IC50: 1.1 x 10(-7) M) also blocked the inhibitory action of melatonin. These results suggest that melatonin may interact with an apamin-sensitive, possibly Ca(2+)-activated, K+ channel and thus cause an inhibition of ileal smooth muscle contractions.

calan drug classification

In this study, our goal was to develop an efficient in situ test adapted to screen hepatotoxicity of various chemicals, a process which remains challenging during the early phase of drug development. The test was based on functional human hepatocytes using the HepaRG cell line, and automation of quantitative fluorescence microscopy coupled with automated imaging analysis. Differentiated HepaRG cells express most of the specific liver functions at levels close to those found in primary human hepatocytes, including detoxifying enzymes and drug transporters. A triparametric analysis was first used to evaluate hepatocyte purity and differentiation status, mainly detoxication capacity of cells before toxicity testing. We demonstrated that culturing HepaRG cells at high density maintained high hepatocyte purity and differentiation level. Moreover, evidence was found that isolating hepatocytes from 2-week-old confluent cultures limited variations associated with an ageing process occurring over time in confluent cells. Then, we designed a toxicity test based on detection of early mitochondrial depolarisation associated with permeability transition (MPT) pore opening, using JC-1 as a metachromatic fluorescent dye. Maximal dye dimerization that would have been strongly hampered by efficient efflux due to the active, multidrug-resistant (MDR) pump was overcome by coupling JC-1 with the MDR inhibitor verapamil. Specificity of this test was demonstrated and its usefulness appeared directly dependent on conditions supporting hepatic cell competence. This new hepatotoxicity test adapted to automated, image-based detection should be useful to evaluate the early MPT event common to cell apoptosis and necrosis and simultaneously to detect involvement of the multidrug resistant pump with target drugs in a human hepatocyte environment.

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All the implants were removed from animal body 4 weeks later for study. For the fibroblasts activity study, another 10 days of cell culture was done. The viability and proliferation of HSc fibroblasts in group C mice were significantly decreased at 10 days after explantation. The fibroblast numbers in the 3 groups were as follows: (A) 16.6×10⁵; (B) 1.5×10⁵; and (C) 0.4×10⁵ (P<0.05). At 4 weeks after implantation, group C showed the significantly least amount of type I collagen (A, 0.12 μg/mL; B, 0.07 μg/mL; C, 0.055 μg/mL; P<0.05). In the nonimplanted scars, the collagen in group C was 0.4 μg/mL, less than that in groups B (0.6 μg/mL) and A (1.7 μg/mL; P<0.05). Significant differences were observed in reduction of scar weight among the 3 groups (A, 85%; B, 82.3%; C, 78.6%; P<0.05). The combination therapy group, that is, group C, significant inhibition of FPCL contraction and delayed contraction of burn scar fibroblasts compared with the other groups. The FPCL contraction rate at 4 weeks in groups A, B, and C was 15.4%, 65%, and 73.4% of the original size, respectively (P<0.05).

calan 120 mg

Treatment of Bacillus licheniformis cultures with biotic oligosaccharide elicitors is known to increase the production of the antibiotic bacitracin A. The mechanism of the elicitation is currently under investigation and in this paper we provide evidence on the modulatory role of Ca(2+) ions during this process. Addition of elicitors, mannan oligosaccharides, oligoguluronate and oligomannuronate to the liquid cultures resulted in 9.0, 5.2 and 5.0% increase in cytosolic Ca(2+) levels in B. licheniformis, while the presence of verapamil (Ca(2+) channel blocker) resulted in 74% decrease in bacitracin A levels, as compared to the control culture. We propose that Ca(2+) ions may acts as a secondary messenger in the regulation of the bacitracin A synthesis in the elicited B. licheniformis cultures.

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EFV should not modify intestinal absorption of co-administered substrates of P-gp, but could decrease plasma concentrations of co-administered drugs metabolized by P450.

calan 180 mg

Ebola virus causes sporadic outbreaks of lethal hemorrhagic fever in humans, but there is no currently approved therapy. Cells take up Ebola virus by macropinocytosis, followed by trafficking through endosomal vesicles. However, few factors controlling endosomal virus movement are known. Here we find that Ebola virus entry into host cells requires the endosomal calcium channels called two-pore channels (TPCs). Disrupting TPC function by gene knockout, small interfering RNAs, or small-molecule inhibitors halted virus trafficking and prevented infection. Tetrandrine, the most potent small molecule that we tested, inhibited infection of human macrophages, the primary target of Ebola virus in vivo, and also showed therapeutic efficacy in mice. Therefore, TPC proteins play a key role in Ebola virus infection and may be effective targets for antiviral therapy.

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Detectable levels of troponins are often found in serum of patients with atrial fibrillation (AF), and recent reports suggest that Tn concentrations are independently related to patient prognosis.

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Unlike in verapamil and metoprolol poisoning models, levosimendan did not improve CO or survival in propranolol poisoning. Epinephrine improved BP, but not CO, suggesting that its actions were due to peripheral vasoconstriction.

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A single-pass "four-site" rat intestinal perfusion model and a cultured Caco-2 cell model were employed.

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Among new taxoids, taxuspines A-H and J-T, and known taxoids containing taxol and taxol-type compounds with an N-acylphenylisoserine group at C-13 and an oxetane ring at C-4 and C-5 isolated from stems and leaves of the Japanese yew Taxus cuspidata Sieb. et Zucc., two non-taxol-type compounds remarkably reduced CaCl2-induced depolymerization of microtubules. Furthermore, seven non-taxol-type compounds increased cellular accumulation of vincristine in multidrug-resistant(MDR) tumor cells as potent as verapamil, while taxol and taxol-type compounds did not show such an activity. In addition, the non-taxol-type compounds enhancing vincristine accumulation inhibited competitively binding of azidopine to P-glycoprotein. These results suggest that some non-taxol-type taxoids may be useful for overcoming MDR in tumor cells.

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Single centre at a university hospital.

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The study consisted of six groups (N=30; five rabbits/group): (1) Control with no pretreatment, monocrotaline injected groups: (solutions were perfused following termination of CPB for 60 min); (2) Control for pulmonary hypertension (PHT); (3) isoproteronol; (4) VIP 10(-6) M; (5) VIP 10(-5) M; (6) nitroglycerine. Normothermic CPB was instituted in thirty rabbits at a flowrate of 100 ml/kg/min for 120 min. Heart rate, mean arterial pressure (MAP), central venous, left atrium (LAP), pulmonary artery (PAP) pressures, pulmonary resistance (Rp), blood gases and ions were measured before and 15, 30, 45 and 60 min after CPB. The VIP 10(-5) M group was subjected to an additional 1.7 x 10(-6) M propranol and 2 mM verapamil infusions for a further 15 min.

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Average time to death was 21.0±9.57 minutes for group C, 35.57±10.61 minutes for group S, 37.14±16.6 minutes for group L and 49.86±27.56 minutes for group SL. Time to death was significantly longer in other groups than in the control group (p<0.05).

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An endovascular treatment of vasospasm following a subarachnoid aneurysmal haemorrhage is to be implemented if the patient presents clinical or biological symptoms arguing for brain ischemia in conjunction with increased Doppler velocities despite well controlled systemic haemodynamic. Treatment might be either pharmacological or haemodynamic. Calcium and phosphodiesterase inhibitors can be administered. The former could also provide a neuroprotective effect as compared to the latter. In Europe, nimodipine is widely used whereas nicardipine and verapamil are the major molecules administered in North America where iv nimodipine is not FDA approved. Papaverine is less used nowadays because of its short duration of action and of the risk of aggravation of raised intracranial pressure. Balloon angioplasty has a long lasting effect but can be applied only to proximal spasm. Complications of its use are rare but life threatening. In some cases, both the pharmacological approach and the mechanical approach are used in combination.

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In 6 healthy volunteers a multilumen perfusion catheter was used to generate a 20-cm isolated jejunal segment that was perfused with 80 mg verapamil. Simultaneously, 5 mg [(2)H(7)]verapamil was given intravenously. Blood, perfusate, and bile samples were analyzed for parent verapamil and its major metabolites.

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The cerebrovascular selectivity and vasospasmolytic action of AJ-3941 ((+/-)-(E)-1-(3-fluoro-6, 11-dihydrodibenz[b,e]oxepin-11-yl)-4-(3-phenyl-2-propenyl)-p iperazine dimaleate. CAS 143110-70-7), a new calcium antagonist, were studied in isolated rabbit and dog arterial preparations. In rabbit arterial ring preparations, AJ-3941 dose-dependently inhibited the contractions of various arteries caused by high K(+)-depolarization (high K+) and prostaglandin F2 alpha (PG). The inhibitory potency of AJ-3941 varied in different arteries, in descending order as follows: high K+: basilar > coronary > femoral > renal > mesenteric artery, PG: basilar > coronary > > femoral and renal artery. The median inhibitory concentration (IC50) in the basilar artery was over 40 times lower than that in the mesenteric or femoral artery for which the weakest inhibition in the examined arteries was observed. This selective action of AJ-3941 for cerebral artery was also observed in the frontal and middle cerebral arteries of dogs. The selectivity for the rabbit basilar artery was higher than those of flunarizine and nicardipine. Additionally, the contractile response of the rabbit basilar artery induced by phorbol 12,13-dibutyrate (PDBu), an activator of protein kinase C (PKC), was greater than those of the arteries examined such as the coronary, femoral and mesenteric arteries. The response in the basilar artery was greatly reduced in Ca(2+)-free medium, while this was not the case in other arteries. AJ-3941 as well as H-7, an inhibitor of PKC, potently inhibited PDBu-induced contractile response in the basilar artery in the presence, but not in the absence of Ca2+ in the medium, whereas the existing calcium antagonists, diltiazem and nicardipine, did not inhibit the contractile response in both conditions. These results suggest that the PKC-dependent system which is mediated by influx of extracellular Ca2+ profoundly contributes to the contraction of the cerebral artery and that the cerebroselective-vasodilating effect of AJ-3941 may depend, at least partly, on the inhibition of the PKC-mediated contractile response. In rabbit basilar arteries, AJ-3941 caused a dose-dependent inhibition of the contraction induced by various vasospasmogens, such as endothelin-1 (ET), arachidonic acid, 15-hydroperoxy-eicosatetraenoic acid and the thromboxane A2-mimetic U-46619. Furthermore, when isolated basilar arteries of the dog were perfused intraluminally with AJ-3941 at the concentration that inhibits high K(+)- or PG-induced contraction in the rabbit basilar artery, AJ-3941 effectively antagonized the vasospasm induced by extraluminal application of PG or ET. However, when flunarizine, nicardipine, diltiazem or verapamil was used for intraluminal perfusion of the same preparations, none of these drugs exerted spasmolytic effect. These results indicate that AJ-3941 has cerebrovascular selective-vasospasmolytic action, and consequently is thought to be effective in cerebrovascular disorder such as vasospasm following subarachnoid hemorrhage.

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In the porcine model, intraluminal application of pharmacologic agents produced independent effects on ureteral dilation and peristalsis. Theophylline inhibited ureteral peristalsis, and verapamil produced acute proximal-ureteral dilation. The ability to alter ureteral diameter or peristaltic activity acutely may facilitate ureteroscopy.

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Cluster headache is a primary headache with a male predominance that presents in two forms: episodic and chronic, occurring at 45-to 60-day intervals with one to three headaches a day lasting 45 min to 2 h. An attack starts by a violent unilateral retro-ocular pain with sympathetic signs such as tearing and rhinorrhea. Diagnosis is made by questioning and therefore requires no complementary tests. Treatment for the attack consists of injectable sumatriptan or oxygen therapy, with long-term treatment with verapamil, lithium salts, or Topiramate; in certain cases in which the number of attacks is greater than two, injections of corticosteroids at the emergence of the Arnold nerve can be used, or in cases of attacks resistant to all treatments, hypothalamus stimulation surgery can be useful.

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Parkinson's disease (PD) is associated with a loss of neurons from the midbrain. The cause of PD is unknown, but it is established that certain neurotoxins can cause similar syndromes. The brain is normally protected from these noxious blood-borne chemicals by the blood-brain barrier which includes specialized proteins on the inside of blood vessels in the brain. These act as molecular efflux pumps and P-glycoprotein (P-gp) is an abundant representative. Vulnerability to PD appears codetermined by the genotype for the P-gp gene. We hypothesized that PD patients have reduced P-gp function in the blood-brain barrier. We used positron emission tomography to measure brain uptake of [(11)C]-verapamil, which is normally extruded from the brain by P-gp. Here, we show significantly elevated uptake of [(11)C]-verapamil (18%) in the midbrain of PD patients relative to controls. This is the first evidence supporting a dysfunctional blood-brain barrier as a causative mechanism in PD.

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calan generic name 2016-01-10

Cardiac memory (CM) can be induced by both short and long period buy calan of pacing from the right ventricle. Although several mechanisms have been proposed in animal studies, mechanisms of CM in humans are not well studied.

calan 180 mg 2017-12-29

Determining the effect of a compound on I (Kr) is a standard screen for drug safety. Often the effect is described using a single IC(50) value, which is unable to capture complex effects buy calan of a drug. Using verapamil as an example, we present a method for using recordings from native myocytes at several drug doses along with qualitative features of I (Kr) from published studies of HERG current to estimate parameters in a mathematical model of the drug effect on I (Kr). I (Kr) was recorded from canine left ventricular myocytes using ruptured patch techniques. A voltage command protocol was used to record tail currents at voltages from -70 to -20 mV, following activating pulses over a wide range of voltages and pulse durations. Model equations were taken from a published I (Kr) Markov model and the drug was modeled as binding to the open state. Parameters were estimated using a combined global and local optimization algorithm based on collected data with two additional constraints on I (Kr) I-V relation and I (Kr) inactivation. The method produced models that quantitatively reproduce both the control I (Kr) kinetics and dose dependent changes in the current. In addition, the model exhibited use and rate dependence. The results suggest that: (1) the technique proposed here has the practical potential to develop data-driven models that quantitatively reproduce channel behavior in native myocytes; (2) the method can capture important drug effects that cannot be reproduced by the IC(50) method. Although the method was developed for I (Kr), the same strategy can be applied to other ion channels, once appropriate channel-specific voltage protocols and qualitative features are identified.

calan 40 mg 2015-03-17

P-glycoprotein (P-gp)-mediated chemoresistance plays an important buy calan role in drug resistance.

calan 240 mg 2016-10-22

Angioplasty using distal filter protection (Angioguard, Cordis, Warren, NJ, USA) was attempted in 38 buy calan patients (mean age 65 +/- 11 years, 79% males) affected by ACS. A percutaneous coronary intervention was performed in 27 native coronary arteries, in 10 SVG and in one arterial graft (mean diameter stenosis 88 +/- 9%). Patients with vessels presenting severe proximal tortuosity, more than mild calcification, a diameter < 3.0 mm and a lesion length > 15 mm were excluded.

calan tablets 2016-12-06

The purpose of the study was to evaluate several n-in-one cocktails of heterogeneous compounds to increase the throughput of permeability studies across buy calan Caco-2 monolayers, to investigate the reliability and applicability of the method, and to develop fast and sensitive analysis for the compounds. Compounds with potential interactions in efflux and/or active transport were chosen.

calan drug classification 2016-02-20

It is well known that atrial fibrillation (AF) tends to become permanent with time as illustrated by the fact that it becomes more difficult to maintain sinus rhythm when AF has been present for a long time. Atrial remodelling plays a part in this process and has been studied in experimental models. Atrial remodelling is defined as all the phenomena occurring during AF contributing to its maintenance. The persistence of AF induced by stimulation in the animal depends on the duration and the repetition of the atrial stimulation and it would appear that "AF induces AF". The tendency for AF to persist is associated buy calan with a shortening of the effective atrial refractory period with loss of its adaptation to the heart rate. The determining factor of both electrical and structural remodelling is the rapidity of the atrial rhythm of the AF itself. These phenomena lead to a type L calcium cellular overload as shown by its prevention or attenuation by the administration of verapamil, a calcium antagonist. Electrical remodelling is accompanied by a structural remodelling in the experimental model of persistent AF over several weeks. Samples from the two atria examined by electronic microscopy show mitochondrial changes, an accumulation of glycogen, a deficit in myofibrils, a redistribution of the nuclear chromatim and a reduction of sarcoplasmic reticulum with changes in protein structure. This structural remodelling is a reaction of adaptation similar to that observed in hibernating myocardium during ischaemia and aims to prolong cellular viability by decreasing atrial contractility. Another aspect of structural remodelling is the activation of fibroblasts with formation of fibrosis with resulting heterogeneity of the conduction tissue. There is also an increase in converting enzyme and angiotensin II concentrations. Irbesartan, an angiotensin II antagonist, reduced fibroblast growth. This has clinical applications as shown by the reduction in the recurrences of AF after cardioversion when given in association with amiodarone. Persistent AF leads to left atrial dilatation with abnormal atrial contractility. Further studies are necessary to determine the effect of atrial remodelling which might also act on the foci responsible for inducing the AF. Better understanding of atrial remodelling will contribute to the use of new pharmacological agents to prevent AF.

calan medication 2017-10-06

Patients with heart failure are particularly susceptible to the negative effects of calcium channel blockers because the failing heart demonstrates a defect in the delivery of calcium to the contractile proteins, and an attenuation of the normal sympathetic reflexes. Currently these drugs have no place in the treatment of heart failure caused by systolic dysfunction of the left ventricle. Calcium channel blockers should probably not be described for patients with coronary artery disease and left ventricular dysfunction. When the patient needs additional treatment for angina and beta-blockers or nitrates have not given satisfactory results, it may be appropriate to prescribe amlodipine buy calan or felodipine.

calan 5 mg 2016-08-17

We investigated the in vivo signal-transduction pathways to stimulate phasic contractions in normal and inflamed ileum by close intra-arterial infusions of test substances. Methacholine stimulated phasic contractions dose dependently. This response was suppressed during inflammation. Verapamil inhibited the response to methacholine dose dependently in both normal and inflamed ileum. Neomycin inhibited the response partially in normal ileum and almost completely in inflamed ileum. H-7 and chelerythrine partially inhibited buy calan the methacholine response in normal ileum but had no significant effect in inflamed ileum. Ryanodine stimulated phasic contractions that were blocked by TTX, hexamethonium, atropine, or ruthenium red. Ruthenium red, however, had no significant effect on the contractile response to methacholine.

calan dosage 2016-02-15

Data were to have been independently extracted and analysed on an intention-to-treat basis. The relative risk (RR) and 95% confidence intervals (CI) of homogeneous dichotomous data were to have been calculated using a random effects model, and, where possible, the number needed to treat calculated. Weighted mean differences (WMD) were to have been buy calan calculated for continuous data.

calan sr dosage 2016-08-11

Inositol 1,4,5-trisphosphate (IP(3)) is an important second messenger that can trigger a Ca(2+) wave prolongated between cells. This intercellular signaling was found defective in some gap junction connexin deafness mutants. In this study, the mechanism underlying IP(3) intercellular signaling in the cochlea was investigated. A gap junction channel is composed of two hemichannels. By using a fluorescence polarization technique to measure IP(3) concentration, the authors found that IP(3) could be released by gap junction hemichannels in the cochlea. The IP(3) release was increased about three- to fivefold by the reduction of extracellular Ca(2+) concentration or by mechanical stress. This incremental release could be blocked by gap junction blockers but not eliminated by a purinergic P2x receptor antagonist buy calan and verapamil, which is a selective P-glycoprotein inhibitor inhibiting the ATP-binding cassette transporters. The authors also found that IP(3) receptors were extensively expressed in the cochlear sensory epithelium, including on the cell surface. Extracellular application of IP(3) could trigger cellular Ca(2+) elevation. This Ca(2+) elevation was eliminated by the gap junction hemichannel blocker. These data reveal that IP(3) can pass through hemichannels acting as an extracellular mediator to participate in intercellular signaling. This hemichannel-mediated extracellular pathway may play an important role in long-distance intercellular communication in the cochlea, given that IP(3) only has a short lifetime in the cytoplasm.

calan 120 mg 2017-07-28

The objective of this study was to prepare and evaluate carrageenan beads as a controlled buy calan release system for a freely water soluble drug verapamil hydrochloride and a slightly water soluble drug ibuprofen. Beads were prepared by ionotropic gelation method. The influence of formulation factors (drug content, polymer concentration, counterion type and concentration, outer phase volume) on the particle size, encapsulation efficiency and in vitro release characteristics of beads was investigated. The encapsulation efficiency of veraparnil HCl in the beads (34.8-71.1%) was higher than that of ibuprofen (23.6-58%). While about 30% of ibuprofen was released at 6 h, about 70% of verapamil HCl was released in 5 h from the carrageenan beads prepared.

calan drug 2016-04-02

Prolonged exposure of cells to an agonist of a G-protein-coupled receptor usually results in an attenuation of the cellular response. To elucidate the cellular mechanisms of sensitization or desensitization in an insulin secretory cell system (INS-1 cells), we investigated a regulatory link between G-protein alpha(s)- and alpha(i2)-subunits mRNA, their protein levels and insulin secretion as the biological effect using various compounds. Incubation with epinephrine (50 microM) for 8 h decreased alpha(s)- and alpha(i2)-mRNA levels to 58% and 72%, respectively, which is reversed after a longer incubation. From results using isoprenaline and the alpha2-agonist UK 14,304 epinephrine is shown to mediate its actions via alpha2- but not beta-adrenoceptors. The insulin inhibitory neuropeptide galanin (50 nM) caused a decrease of alpha(s)- and alpha(i2)-mRNA levels, whereas insulinotropic compounds (incretin hormones) such as GIP or GLP-1 (both 10 nM) led to an increase of alpha(s)- and alpha(i2)-mRNA levels. By using the Ca2+ channel blocker verapamil (50 microM) alpha(i2)-mRNA changes clearly depend on Ca2+ influx. The effects on alpha(i2)-mRNA were accompanied by a parallel, albeit weaker effect on the protein level (only GIP and UK 14,304 were investigated). The changes in buy calan alpha(i2)-mRNA levels by either compound were paralleled by inverse changes in insulin secretion: preincubation with UK 14,304 for 8 h led to an increased insulin secretion when challenged by either GLP-1, GIP or glucose (8.3 mM). This was similar for galanin, another potent inhibitor of insulin release. On the other hand, exposure to the incretins GIP or GLP-1 for 8 h induced a smaller insulin release when challenged afterwards by either UK 14,304, galanin, GIP, GLP-1, or glucose. Thus the influence on insulin secretion of various compounds is reciprocal to the regulation of alpha(i2)-mRNA levels but not alpha(s)-mRNA levels. There is, therefore, evidence from all the manoeuvres used that alpha(i2)-mRNA regulation may play a role in heterologous sensitization and desensitization of insulin secretion.

calan 80 mg 2016-12-14

Drug-drug interactions (DDIs) and associated toxicity from cardiovascular drugs represents a major problem for effective co-administration of cardiovascular therapeutics. A significant amount of drug toxicity from DDIs occurs because of drug interactions and multiple cardiovascular drug binding to the efflux transporter P-glycoprotein (Pgp), which is particularly problematic for cardiovascular drugs because of their relatively low therapeutic indexes. The calcium channel antagonist, verapamil and the cardiac glycoside, digoxin, exhibit DDIs with Pgp through non-competitive inhibition of digoxin transport, which leads to elevated digoxin plasma concentrations and digoxin toxicity. In the present study, verapamil-induced ATPase activation kinetics were biphasic implying at least two verapamil-binding sites on Pgp, whereas monophasic digoxin activation of Pgp-coupled ATPase kinetics suggested a single digoxin-binding site. Using intrinsic protein fluorescence and the saturation transfer double difference (STDD) NMR techniques to probe drug-Pgp interactions, verapamil was found to have little effect on digoxin-Pgp interactions at low concentrations of verapamil, which is consistent with simultaneous binding of the drugs and non-competitive inhibition. Higher concentrations of verapamil caused significant disruption of digoxin-Pgp interactions that suggested overlapping and competing drug-binding sites. These interactions correlated to drug-induced conformational changes deduced from acrylamide quenching of Pgp tryptophan fluorescence. Also, Pgp-coupled ATPase activity kinetics measured with a range of verapamil and digoxin concentrations fit well buy calan to a DDI model encompassing non-competitive and competitive inhibition of digoxin by verapamil. The results and previous transport studies were combined into a comprehensive model of verapamil-digoxin DDIs encompassing drug binding, ATP hydrolysis, transport and conformational changes.

calan overdose 2017-08-06

The article deals with usage of nondihydropiridine calcium antagonists--verapamil and dilthiasem--in treating patients with arterial hypertension, cardiomyopathy and arrhythmia, for secondary prevention of IHD. Data also concern cardio-, angio--and nephroprotective activity of the medications, their ability to prevent left ventricle hypertrophy, possible usage in patients after myocardial infarction. The authors also discuss problems of tolerance and safety of calcium antagonists with prolonged action vs. those with buy calan short-term action.

calan sr medication 2015-06-05

The biflavone amentoflavone is an ingredient of Hypericum perforatum L. (Clusiaceae), a plant which is widely used for the treatment of mild to moderate depression. Amentoflavone inhibits the binding of flumazenil to the benzodiazepine binding site of the GABA A -receptor (IC(50) = 14.9 nM). Since it has to pass the blood-brain barrier (BBB) before reaching this receptor, the Seroquel Overdose penetration of [(3)H]-amentoflavone through BBB was studied in an in vitro model consisting of primary cell cultures of porcine brain capillary endothelial cells (BCEC). Concentration-dependent uptake (37-2000 nM) was neither saturable nor temperature-sensitive indicating passive diffusion as the major uptake mechanism. This finding was confirmed by transport experiments through BCEC monolayers (> 2 % of applied dose was transported after 30 min). Co-administration of Hypericum extract increased amentoflavone transport significantly (amentoflavone alone: permeability coefficient P(app) = 4.59.10(-6) cm/s; co-administrated sucrose: P(app) = 3.22.10(-6)cm/s; amentoflavone together with hypericum: P(app) = 6.74.10(-6)cm/s, co-administrated sucrose P(app) = 5.49.10(-6)cm/s) indicating that Hypericum constituents enhance amentoflavone transport possibly by modulating paracellular permeability. Experiments with the P-glycoprotein (P-gp) overexpressing cell line P388-MDR showed that amentoflavone uptake was significantly enhanced by addition of the P-gp inhibitor verapamil, suggesting a P-gp mediated back-transport out of the cells. In conclusion, our findings show, that amentoflavone is able to pass the blood-brain barrier in vitro by passive diffusion.

calan eeze review 2015-03-04

N-type Ca2+ channel is Inderal Drug strongly suggested in CA1 pyramidal neuron in rat hippocampal slices.

calan pill 2017-08-09

The aim of this study was to assess potential differences Azulfidine Mg in the 24-h antihypertensive response to treatment with the controlled-onset, extended-release (COER) calcium antagonist, verapamil in men versus women and older versus younger patients with hypertension.

calan tab 2015-12-30

Apart from the Norvasc 5mg Medication IHS criteria additional features like nausea/vomiting and migrainous aura may guide the diagnosis of CH. A large number of CH patients do not receive adequate treatments.

calan dosage forms 2015-09-09

Equilibrium dialysis and high-performance liquid chromatography were used to analyze the binding rates of the two medicines to serum protein. The interactions based on bovine serum albumin (BSA) and human serum albumin (HSA) were investigated by using spectrofluorimetry. The interaction mode of arenobufagin and verapamil hydrochloride binding to serum proteins was Voltaren Max Dose simulated by molecular docking.

calan reviews 2015-07-20

In many patients with obstructive hypertrophic cardiomyopathy, an abrupt mid-systolic drop in left ventricular ejection velocity can be detected. We analyzed 27 patients with obstructive hypertrophic cardiomyopathy who had 43 echocardiographic examinations (mean gradient 53 +/- 6 mm Hg). Exams showing a mid-systolic drop had higher mean outflow tract pressure gradients (90 +/- 6 compared with 29 +/- 4 mm Hg, p < 0.001). After medical elimination of obstruction, the mid-systolic drop was Cardura Dosage Strengths no longer seen. We measured 105 pulsed-wave Doppler tracings in the left ventricular cavity and compared them with 90 continuous-wave tracings through the outflow tract. There was a close temporal correlation between the nadir of the left ventricular velocity drop and the peak continuous-wave left ventricular outflow tract velocity (r = 0.99). There was also a close temporal correlation between the onset of the fall in pulsed velocity and the onset of M-mode mitral-septal contact (r = 0.95).

calan generic name 2016-09-25

Retrospective study of 257 patients (152 male and 105 female, 1,171 patient-years) with RAI diagnosed between 1980 and 2005.

calan 180 mg 2017-07-11

Endocardial pacing leads were implanted in the right ventricle, right atrium, and coronary sinus in 18 dogs. The right ventricular lead was connected to an implanted pacemaker capable of rapid ventricular pacing. The atrial leads were used to perform electrophysiologic studies in conscious animals at baseline in all dogs, during CHF induced by rapid ventricular pacing at 235 beats/min in 15 dogs, and during recovery from CHF in 6 dogs. After 20 +/- 7 days of rapid ventricular pacing, inducibility of sustained atrial tachycardia (cycle length 120 +/- 12 msec) was enhanced in dogs with CHF. Atrial tachycardia required a critical decrease in atrial burst pacing cycle length (< or = 130 msec) for induction and often could be terminated by overdrive pacing. Calcium antagonists (verapamil, flunarizine, ryanodine) terminated atrial tachycardia and suppressed inducibility. Effective refractory periods at 400- and 300-msec cycle lengths in the right atrium and coronary sinus were prolonged in dogs with CHF. Atrial cells from dogs with CHF had prolonged action potential durations and reduced resting potentials and delayed afterdepolarizations (DADs). Mitochondria from atrial tissue from dogs with CHF were enlarged and had internal cristae disorganization.

calan 40 mg 2017-06-20

We assessed the role of endothelium in the arterial response to thapsigargin, the Ca(2+)-ATPase inhibitor of the endoplasmic reticulum, in rat isolated aortic rings. Thapsigargin induced an endothelium-dependent relaxation of phenylephrine-contracted aortic rings with an EC(50) of 2.6+/-0.4 nM and a 75% maximum relaxation, while it was less effective against 30 mM K(+)-induced contraction. Pretreatment of aortic rings with N(G)-nitro-L-arginine methyl ester (30 microM) or methylene blue (1 microM) reduced thapsigargin-induced relaxation by approximately 85%. Thapsigargin failed to relax the endothelium-denuded rings. L-Arginine (3 mM) partially, but significantly, antagonized the effect of 30 microM N(G)-nitro-L-arginine methyl ester. Pretreatment with indomethacin (3 microM), glibenclamide (1 microM) or iberiotoxin (100 nM) did not alter the thapsigargin-induced relaxation. In contrast, pretreatment with tetrapentylammonium ions (TPA(+), 1-3 microM) or with 300 microM Ba(2+) suppressed the relaxant response to thapsigargin. TPA(+) (3 microM) also attenuated acetylcholine-induced relaxation. Thapsigargin-induced endothelium-dependent relaxation was primarily dependent on the presence of extracellular Ca(2+). Interestingly, when the tissues were exposed to very low concentrations of thapsigargin (1-3 nM) the nitric oxide-dependent relaxation induced by acetylcholine or A23187 was markedly reduced. While thapsigargin (3 nM) did not influence the relaxation induced by endothelium-independent dilators, sodium nitroprusside and verapamil. These results indicate that thapsigargin produced complex vascular effects primarily by acting on the endothelial cells. Thapsigargin causes an endothelial nitric oxide-dependent relaxation; on the other hand, it inhibits nitric oxide-mediated relaxation at the similar concentrations. Activation of TPA(+)- and Ba(2+)-sensitive but not Ca(2+)-activated or ATP-sensitive K(+) channels may be also involved in thapsigargin-induced relaxation of rat isolated aortic rings.

calan 240 mg 2016-10-27

This prospective, double-blind, randomized, controlled trial involved patients, aged 18 to 75 years, with new-onset (< 48 hours) atrial fibrillation who presented to a community-based urban hospital with an annual ED census of 65,000. Exclusion criteria included ventricular response rate lower than 100 or higher than 200 beats/minute, allergy to study drugs, hypotension with evidence of end-organ hypoperfusion, and conduction abnormalities. Consenting patients were randomly assigned to receive rapid digitalization (1.0 mg over 2 hours) or i.v. verapamil (sequential 5-mg boluses up to 20 mg). After ventricular rate was controlled (< 100 beats/minute), oral quinidine (200 mg) was initiated and repeated every 2 hours until conversion to normal sinus rhythm (NSR) occurred, until 1 g of quinidine was administered, or until adverse effects supervened. Heart rate, blood pressure, cardiac rhythm, time to conversion, and adverse effects were documented.

calan tablets 2016-07-29

Comparison of the effect of tocolytic drugs on isolated swine uterus preparations.

calan drug classification 2015-12-24

Verapamil was added to the antiepileptic drug regimen of a 24-year-old woman with intractable epilepsy. The average time interval between hospitalizations for complex partial status doubled. The addition of verapamil greatly improved overall seizure control and subjective quality of life in this pharmacoresistant patient.

calan medication 2017-07-25

ATP-binding cassette (ABC) transporters are membrane-bound proteins involved in the movement of various substrates, including drugs and insecticides, across the lipid membrane. Demonstration of the role of human ABC transporters in multidrug resistance has led to speculation that they might be an important mechanism controlling the fate of insecticides in insects. However, the role of ABC transporters in insects remains largely unknown. The small brown planthopper, Laodelphax striatellus Fallén, has developed resistance to most of the insecticides used for its control. Our goals were to identify the ABC transporters in La. striatellus and to examine their involvement in resistance mechanisms, using related strains resistant to chlorpyrifos, deltamethrin and imidacloprid, compared with the susceptible strain. Based on the transcriptome of La. striatellus, 40 full-length ABC transporters belonging to the ABCA-ABCH subfamilies were identified. Quantitative PCR revealed that over 20% of genes were significantly up-regulated in different resistant strains, and eight genes from the ABCB/C/D/G subfamilies were up-regulated in all three resistant strains, compared with the susceptible strain. Furthermore, synergism studies showed verapamil significantly enhanced insecticide toxicity in various resistant strains but not in the susceptible strain. These results suggest that ABC transporters might be involved in resistance to multiple insecticides in La. striatellus.

calan 5 mg 2016-10-17

Phagocytes play a major role in several diseases. In particular mononuclear phagocyte-derived foam cells have a prominent role in the development of the atherosclerotic lesions. Macrophages are present in all stages of atherogenesis; they internalize lipoproteins and accumulate cholesterol. Moreover, lipid-filled macrophages, by secreting extracellular matrix-degrading enzymes, may weaken rupture-prone atherosclerotic plaques, thus increasing the probability of precipitating atherosclerotic acute symptoms (i.e., myocardial infarction, angina, etc.). Therefore, control of cellular functions and cholesterol accumulation in macrophages represent pharmacological targets against atherosclerosis. In our laboratory we studied the effect of calcium antagonists on cellular cholesterol esterification in cultured macrophages. We also demonstrated that the HMG-CoA reductase inhibitors (vastatins) fluvastatin and simvastatin prevented cholesterol deposition in cultured human and murine macrophage by inhibiting modified LDL endocytosis. Interestingly, vastatin activity was more pronounced in cholesterol-loaded macrophages (i.e., foam cells) than in normal cells. In conclusion, in vitro pharmacological control of cholesterol accumulation in macrophages may be achieved with some calcium antagonists and vastatins independently of their effects on blood pressure or cholesterolemia.

calan dosage 2017-08-04

This study investigated fexofenadine (FXD) transport and the inhibition of FXD transport in Caco-2 cell monolayer transwells, using rhodamine 123 (RH123) transport as a positive control. FXD transport from the basolateral (B) to apical (A) compartment was fivefold higher than A to B transport. FXD transport was linear with respect to time (up to 270 min) and concentration (up to 300 microm). Similar results were seen with the positive control RH123. Ritonavir (100 PM) and verapamil (100 microm) reduced transport of FXD and RH123 by more than 80%, whereas transport was not inhibited by 100 m indomethacin or 2 mM probenecid. This suggests predominantly P-glycoprotein (P-gp)-mediated transport as opposed to transport by multidrug resistance protein. In concentration-response experiments, FXD transport was inhibited by verapamil and ritonavir with IC50 values of 6.5 microm and 5.4 microm, respectively. Results from this in vitro study demonstrate differential transport of FXD across Caco-2 cell monolayers and inhibition of FXD transport by established P-gp inhibitors. Thefindings support the use of FXD as an index or probe compound to reflect P-gp activity in vivo.

calan sr dosage 2016-11-26

Seven male and 2 female patients, seen between July 2004 and February 2005, and between the ages of 32 and 56, are reported with histories of treatment resistant cluster headaches accompanied by borderline low or low serum testosterone levels. The patients failed to respond to individually tailored medical regimens, including melatonin doses of 12 mg a day or higher, high flow oxygen, maximally tolerated verapamil, antiepileptic agents, and parenteral serotonin agonists. Seven of the 9 patients met 2004 International Classification for the Diagnosis of Headache criteria for chronic cluster headaches; the other 2 patients had episodic cluster headaches of several months duration. After neurological and physical examination all patients had laboratory investigations including fasting lipid panel, PSA (where indicated), LH, FSH, and testosterone levels (both free and total). All 9 patients demonstrated either abnormally low or low, normal testosterone levels. After supplementation with either pure testosterone in 5 of 7 male patients or combination testosterone/estrogen therapy in both female patients, the patients achieved cluster headache freedom for the first 24 hours. Four male chronic cluster patients, all with abnormally low testosterone levels, achieved remission.