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Norvasc (Amlodipine)

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Norvasc is an effective strong preparation which is taken in treatment of angina and hypertension diseases. Norvasc acts as an anti-angina and anti-hypertension remedy. Norvasc operates by reducing blood pressure and regulating chest pain through blood provision to the heart.

Other names for this medication:
Abesyl, Abis, Abloom, Actapin, Amlodigamma, Amlodil, Amlodilan, Amlodin, Amlodine, Amlodinova, Amlotens, Amlotop, Amlovas, Amlovasc, Amlovask, Amlow, Amlozek, Amocal, Amodipin, Amonex, Amparo, Ampin, Amtas, Amtim, Amvasc, Amze, Anexa, Angiofilina, Angiovan gmp, Angipec, Anlodipin, Anlow, Antacal, Apitim, Apo-amlo, Apo-amlodipine, Arteriosan, Arterium, Asomex, Astudal, Atloma, Avistar, Balarm, Beglaryl, Calbloc, Calchek, Cardisan, Cardivas, Cardivask, Ciplavasc, Cordi cor, Cordil, Cordipina, Coroval, Cristacor, Dafiro, Dafor, Dilopin, Dilotex, Diplor, Divask, Dopin, Dronalden, Duactin, Edidipin, Emlip-5, Emlodin, Emlon, Esam, Eucoran, Evangio, Exforge, Gensia, Goritel, Harmidipin, Hasanlor, Hipertensal, Hipres, Ilduc, Imped, Intervask, Ipin, Istin, Kaprin, Klodip-5, Krudipin, Lama, Lavi-press, Locard, Lodepine, Lodimax, Lodipar, Lodipin, Lodipin-5, Lodipine, Lofral, Lopin, Lopiten, Lordivas, Monovas, Myodura, Myostin, Naxuril, Newdipine, Nexotensil, Nicord, Nipidol, Nolmoten, Noloten, Nolvac, Novaten, Omelar cardio, Oralcam, Orcal, Orkal, Ozlodip, Pelmec, Perivasc, Perten, Pinam, Presdeten, Presilam, Presovasc, Primodil, Q-spin, Raserdipina, Recotens, Roxflan, Rustin, Sidopin, Sistopress, Stadovas 5, Stamlo, Suplar, Tenox, Tensigal, Tensivask, Tensocard, Terloc, Tervalon, Theravask, Toraass a, Vamlo, Vascam, Vasocal, Vasocard, Vasonorm, Vasopin, Vazkor, Vazotal, Vilpin, Xelcard, Zeppeliton, Zorem, Zundic

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Also known as: Amlodipine.


Norvasc is created by pharmacy specialists to combat angina and hypertension diseases. Target of Norvasc is to control chest pain and decrease level of blood pressure.

Norvasc acts as an anti-angina and anti-hypertension remedy. Norvasc operates by reducing blood pressure and regulating chest pain through blood provision to the heart. You can take Norvasc in combination with other anti-hypertension preparations.

Norvasc is also known as Amlodipine besylate, Amlip, Avacard, Dailyvasc, Istin, Perivasc.

Norvasc is calcium channel blocker.

Generic name of Norvasc is Amlodipine.

Brand name of Norvasc is Norvasc.


You should take it by mouth.

It is better to take Norvasc once a day at the same time.

Norvasc treats angina and hypertension diseases and can be used both by adults and by children.

Children of 6-17 years:

Starting dosage is 2.5-5 mg.

People with vasospastic angina or coronary artery disease:

Starting dosage is 5-10 mg.

Elderly people, people with hepatic:

Starting dosage is 2.5 mg.

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


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


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children in a container that small children cannot open.

Side effects

The most common side effects associated with Norvasc 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 Norvasc if you are allergic to Norvasc components.

Do not take Norvasc if you're pregnant or you plan to have a baby. Do not use it if you are a nursing mother.

Do not use Norvasc in case of suffering from significant aortic stenosis, cardiogenic shock, and unstable angina.

Try to be careful with Norvasc usage in case of having liver disease, heart failure or hepatic impairment.

Do not use potassium supplements or salt substitutes.

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 Norvasc suddenly.

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To assess the relationship between home blood pressure and left ventricular mass, we evaluated cardiac echocardiography in 297 hypertensive subjects (188 men and 109 women; mean age, 62.8+/-10.3 years) who were treated with amlodipine monotherapy over 1 year (mean dose, 5.5+/-2.3 mg/day). The morning hypertension group (n=57; 19.2%), who had a morning home systolic blood pressure (HSBP) > or =135 mmHg and an evening HSBP <135 mmHg, had a significantly greater left ventricular mass index (LVMI) concomitant with an increase in the homeostasis model assessment insulin resistance index (HOMA-IR) compared to the good control group (n=174; 58.6%), whose morning and evening HSBP were both <135 mmHg, and had a LVMI roughly equivalent to that of the poor control group (n=63; 21.2%), whose morning and evening HSBP were both > or =135 mmHg. By grouping of subjects according to the difference between morning and evening HSBP (delta HSBP), subjects with a delta HSBP> or =10 mmHg had a significantly greater LVMI than subjects with a delta HSBP <10 mmHg. Increases in LVMI in these patients were still significant after adjustment for age, gender, dose of amlodipine, alcohol consumption, body mass index, office systolic blood pressure, and morning and evening HSBP. In a stepwise multivariate regression analysis, delta HSBP (r2=36.2%, p <0.001), morning HSBP (r2=5.5%, p <0.001), HOMA-IR (r2=1.4%, p=0.016) and age (r2=1.0%, p=0.026) were determined to be significant contributing factors for LVMI. This regression model could explain 44.1% of LVMI variability. These results suggest that morning rise in blood pressure is a dominant predictor of left ventricular hypertrophy.

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The JEWEL program consists of two 16-week, international, open-label, multicenter, titration-to-goal studies in patients with hypertension and dyslipidemia. The 2 studies differ based on country of enrollment and certain tertiary endpoints, but the overall designs are very similar. Patients have been enrolled from 255 centers across Canada and 13 European countries. The study is designed to assess the efficacy, safety, and utility of amlodipine/atorvastatin single-pill therapy in a real-world setting. Patients will be initiated at a dose of amlodipine 5 mg/atorvastatin 10 mg, unless previously treated, and will be uptitrated as necessary. The primary efficacy parameter is the percentage of patients, at different levels of cardiovascular risk, achieving country-specific guideline-recommended target levels for blood pressure and lipids. A secondary analysis of efficacy measured attainment of the same single goal for blood pressure across all study participants (JEWEL I and II) and the same single goal for LDL-C across all study participants (JEWEL I and II). The program will utilize a newly developed questionnaire to gain better understanding of participants' beliefs and behaviors towards medical treatment of their multiple risk factors. Approximately 2850 patients will be enrolled in the program, which is due to be completed in August 2005.

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This pilot trial demonstrates that both furosemide and amlodipine might have the same effect during pregnancy. However, a large clinical trial is necessary to prove this.

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G-protein β-polypeptide 3 (GNB3) is a β subunit isoform of G-protein that plays important role in signal transduction of membrane G-protein coupled receptors (GPCRs). The GNB3 splice variant C825T (rs5443) is associated with risk for essential hypertension (EH) and efficacy of therapeutic drugs targeting GPCRs. It is unknown whether the polymorphism is associated with blood pressure (BP) response to telmisartan or amlodipine, two widely prescribed antihypertensive drugs.

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The renin-angiotensin-aldosterone system (RAAS) has long been recognized to play a significant role in hypertension pathophysiology. Certain agents that modify the RAAS can control blood pressure and improve cardiovascular outcomes. Aliskiren is the first of a new class of antihypertensive agents known as renin inhibitors.

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We investigated whether the tissue transglutaminase inhibitor cystamine is able to inhibit remodelling of small arteries in vivo, a possibility suggested by recent in vitro experiments.

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Group 3 patients were found to show a preponderance of metabolic disturbances, such as dyslipidemia, obesity, as well as intrarenal arterial lesions and diminished kidney function. In addition, the most pronounced therapy-induced changes in the parameters under study were also observed in Group 3. In particular, resistive index, pulsatility index of interlobar arteries of the kidneys, and serum creatinine levels increased, the frequency of microalbuminuria episodes reduced, and GFR, endothelium-dependent dilation of the brachial artery, and systolic index rose statistically significantly. Group 3 also displayed statistically significant correlations of the resistive index of the interlobar arteries with GFR, urinary albumin excretion, endothelium-dependent vasodilation, and cardiac index.

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These results showed that antibiotic intake might increase the bioavailability of amlodipine by suppressing gut microbial metabolic activities, which could be followed by changes in therapeutic potency. Therefore, coadministration of amlodipine with antibiotics requires caution and clinical monitoring.

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Recent studies have suggested a differential influence of mean pressure and pulse pressure on myocardial infarction and stroke, and differences among the major drugs in their efficacy at preventing these individual endpoints. We hypothesized that antihypertensive drugs have differing influences upon the pulse wave even when their effects on blood pressure are the same. We studied 30 untreated hypertensive patients, aged 28-55 years, who were rotated through six 6-week periods of daily treatment with amlodipine 5 mg, doxazosin 4 mg, lisinopril 10 mg, bisoprolol 5 mg, bendrofluazide 2.5 mg or placebo. The best drug was repeated at the end of the rotation. Blood pressure readings and radial pulse tonometry (by Sphygmocor) were performed at each visit, and blood was taken for measurement of levels of atrial natriuretic peptide and brain natriuretic peptide (BNP). The Sphygmocor derivation of the central aortic pulse wave was used to measure time for transmission of the reflected wave (T(R)) and the augmentation index (AI), which is the proportional increase in systolic pressure due to the reflected wave. There was a dissociation between the effects of the drugs on blood pressure and pulse wave analysis. Bisoprolol caused the greatest falls in blood pressure and T(R), but was the only drug to increase AI. This paradoxical response to bisoprolol was associated with a 3-fold increase in plasma BNP levels. There was a smaller elevation of BNP in women compared with men, as described previously, and this elevation also was associated with significantly higher values of AI. Other drugs reduced AI, and this was associated with a significant decrease in BNP by amlodipine. In conclusion, antihypertensive drugs differ in their short-term effects on augmentation of the systolic pulse wave and secretion of BNP from the heart, regarded as a sensitive measure of strain on cardiomyocytes. These differences may help to explain cause-specific differences in outcome in recent trials.

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Excess salt, via oxidative stress, accelerates stroke, and angiotensin II, via AT1 Propecia Cost Uk receptor, plays a pivotal role in brain superoxide production of SHRSP by excess salt.

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To study patient compliance in hypertensive outpatients amlodipine (5 mg once daily) and slow release nifedipine (20 mg twice daily) were compared in an open, crossover study in general practices. Four methods of assessment for patient compliance (pill count, taking compliance, days with correct dosing, timing compliance) were used in both study arms. For the latter three assessment a special device, the medication Atarax Online event monitoring system, was used to record the time and date of each opening and closure of the container. The compliance of the 320 hypertensive patients with once-daily amlodipine was markedly superior to twice-daily slow release nifedipine. Therapeutic coverage was also significantly better for amlodipine in the hypertensive patients. Amlodipine was better tolerated than nifedipine slow release. Patient compliance and therapeutic coverage with the calcium antagonist amlodipine given once daily was superior to slow release nifedipine b.d. in hypertensive outpatients recruited in general practice.

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Renal transplantation is performed in patients with end stage renal disease as the best treatment plan. However, different complications may occur in these patients due to the direct consequences of Diovan Cost Walmart the renal disease or drug-induced suppression of the body immune system. The main objective of the present study was to compare different oral lesions in patients receiving renal transplantation with the patients undergoing dialysis referred to two hospitals in Tehran, Iran.

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The objective of the present investigation was to develop and evaluate a drug-in-adhesive transdermal patch for S-amlodipine (S-AM) free base. Initial in vitro experiments were conducted to optimize the formulation parameters before transdermal delivery in rats. The effects of the type of adhesive and the content of permeation enhancers on S-AM free base transport across excised rat skin were evaluated. For in vivo studies, patches were administered transdermally to rats while orally administered S-AM in suspension and intravenously administered S-AM solution were used as controls. The plasma level of S-AM following transdermal application could be maintained for 72 h. After transdermal administration to rats, the absolute bioavailability was 88.8% for S-AM free base. After dose normalization, the areas under the plasma concentration-time curve (AUC) and mean Valtrex Generic Brand residence times (MRT) were evidently increased and extended, respectively. This suggests that the transdermal application of S-AM in a drug-in-adhesive transdermal patch may be used for the treatment for hypertension.

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In treatment of CHF in patients Levitra Cost Walgreens with HD amlodipine is at least not inferior to verapamil for elevation of exercise tolerance and superior to verapamil for improvement of LV diastolic function. Amlodipine might be perspective for use in patients with chronotropic incompetence.

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Safety in the drug treatment of hypertension can only be seen in relation to efficacy, which has now come to mean not just blood pressure (BP) reduction but improvements in hard end points including mortality. Information on safety can come from a variety of sources, in an ascending hierarchy, which is as follows: case-control studies, cohort studies, randomized control trials (RCTs), and metaanalyses based on good RCTs. Only in the case of metaanalyses are definite criteria for acceptability established, but evaluation of case-control and cohort studies remains subjective. Despite these reserves about the data sources, it is proposed that the case-control study pointing to the risk of acute myocardial infarction during therapy with short-acting calcium channel blockers (CCBs) can be balanced out by another better more recent study, and by a large cohort study from Israel. In a very elderly population, a well-designed cohort study strongly suggests that short-acting nifedipine can Zovirax Pills Buy be linked to increased mortality and that the specific links may be with a high dose and when the initial BP is less than 160/90 mm Hg. However, initial BP was only available in an unspecified number of patients. The risk of using short-acting verapamil was no more than that of beta-blockade. These differences can be attributed at least in part to the low catecholamine profile of verapamil and the marked rapid adrenergic activation with short-acting nifedipine, which could also explain the adverse effects found when this agent is given to patients with acute coronary syndromes. During the chronic use of long-acting dihydropyridine (DHP) CCBs, most evidence suggests that there is little or no catecholamine activation, or in the case of amlodipine, even a decrease in plasma catecholamine levels. These differences may explain why the expected regression of left ventricular hypertrophy is obtained with long- but not short-acting DHPs. At present the results of several large randomized controlled trials with long-acting CCBs are awaited. In the meantime, when the decision has been made to use a CCB, the preferential choice is for the use of a non-DHP for hypertension with clinical ischemia or for postinfarct hypertension, for a long-acting CCB for the control of left ventricular hypertrophy, and for the DHP amlodipine when there is associated depression of myocardial function.

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This study was designed to test the hypothesis that plasma concentrations of matrix metallo-proteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9), two enzymes that share similar substrate specificity (collagen type IV and V), possibly related to vascular remodelling, are altered in essential hypertension. The second aim of the study was to assess whether chronic antihypertensive treatment with the calcium channel blocker amlodipine would normalize these alterations. To test this hypothesis, we measured plasma concentrations of active MMP-2 and MMP-9 in 42 patients with never-treated essential hypertension and in 25 normotensive control subjects. Measurements were repeated after 6 months of treatment with the calcium channel blocker amlodipine. Baseline values of MMP-2 and MMP-9 were decreased (P=0.01 and 0.002, respectively) in hypertensive patients compared with normotensives. Hypertensive patients with systemic vascular resistances <1440 dyn s/cm(5) exhibited higher values of MMP-2 (P=0.005) and MMP-9 (P=0.001) than hypertensive patients with systemic vascular resistances >1440 dyn s/cm(5). Treated patients attained a nonsignificant increase in MMP-2 plasma concentrations, but a significant increase in MMP-9 plasma concentrations (P=0.01) compared to respective values before treatment. In conclusion, these findings suggest that plasma concentrations of active MMP-2 and MMP-9, mainly related to vascular extracellular matrix metabolism, are depressed in patients with essential hypertension. A 6 month treatment with amlodipine can normalize MMP-9 but not MMP-2 plasma concentrations. The hypothesis that antihypertensive treatment may modulate collagen metabolism remains to be determined by further studies.

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Baseline FPG >5 mmol/l, BMI, and use of an atenolol +/- diuretic regimen were among the major determinants of NOD in hypertensive patients. The model developed from these data allows accurate prediction of NOD among hypertensive subjects.

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Isolated angioedema of the small intestine is a rare entity. The cases described have been related with angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, or C1 esterase inhibitor deficiency. We present a case of small intestine angioedema caused by calcium channel blockers (CCBs) and a review of the literature.