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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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Time-resolved fluorescence spectroscopy showed interaction of both drugs to HSA based on a static quenching mechanism. Subsequently, second-derivative fluorescence spectroscopy presented different values of parameter H in binary and ternary systems, which were suggested that tryptophan was in a more polar environment in the ternary system than in a binary system. Moreover, the polydispersity index and results from mean number measurements revealed that the presence of the second drug caused a decrease in the stability of systems and increased the heterogeneity of complex. It is also, observed that the gradual addition of HSA has led to a marked increase in fluorescence anisotropy (r) of Amlodipine and Aspirin which can be suggested that the drugs were located in a restricted environment of the protein as confirmed by Red Edge Excitation Shift (REES) studies. The isothermal titration calorimetric technique demonstrated that the interaction of the drugs with HSA was an enthalpically-driven process.

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A simple, sensitive, and specific liquid chromatographic method coupled with electrospray ionization (ESI)-mass spectrometry for the determination of amlodipine is developed. After extraction by ethyl acetate using nicardipine as the internal standard, solutes are separated on a C18 column with a mobile phase of methanol-1% HAc (65:35). Detection is performed on an air pressure ionization single quadruple mass spectrometer equipped with an ESI interface and operated in positive-ionization mode. Amlodipine quantitation is realized by computing the peak-area ratio (amlodipine-nicardipine) of the extracts analyzed in single ion monitoring mode (m/z 431 and m/z 480 for amlodipine and nicardipine, respectively) and comparing them with the calibration curve (r = 0.9991).

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Dimethylarginie dimethylaminohydrolase (DDAH) degrades asymmetric dimethylarginine (ADMA), an endogenous nitric oxide (NO) synthase inhibitor, and comprises 2 isoforms, DDAH1 and DDAH2. To investigate the in vivo role of DDAH2, we generated transgenic mice overexpressing DDAH2. The transgenic mice manifested reductions in plasma ADMA and elevations in cardiac NO levels but no changes in systemic blood pressure (SBP), compared with the wild-type mice. When infused into wild-type mice for 4 weeks, ADMA elevated SBP and caused marked medial thickening and perivascular fibrosis in coronary microvessels, which were accompanied by ACE protein upregulation and cardiac oxidative stress. The treatment with amlodipine reduced SBP but failed to ameliorate the ADMA-induced histological changes. In contrast, these changes were abolished in transgenic mice, with a reduction in plasma ADMA. In coronary artery endothelial cells, ADMA activated p38 MAP kinase and the ADMA-induced ACE upregulation was suppressed by p38 MAP kinase inhibition by SB203580. In wild-type mice, long-term treatment with angiotensin II increased plasma ADMA and cardiac oxidative stress and caused similar vascular injury. In transgenic mice, these changes were attenuated. The present study suggests that DDAH2/ADMA regulates cardiac NO levels but has modest effect on SBP in normal conditions. Under the circumstances where plasma ADMA are elevated, including angiotensin II-activated conditions, ADMA serves to contribute to the development of vascular injury and increased cardiac oxidative stress, and the overexpression of DDAH2 attenuates these abnormalities. Collectively, the DDAH2/ADMA pathway can be a novel therapeutic target for vasculopathy in the ADMA or angiotensin II-induced pathophysiological conditions.

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A simple, rapid, and selective HPLC-UV method was developed for the determination of antihypertensive drug substances: amlodipine besilat (AML), olmesartan medoxomil (OLM), valsartan (VAL), and hydrochlorothiazide (HCT) in pharmaceuticals and plasma. These substances are mostly used as combinations. The combinations are found in various forms, especially in current pharmaceuticals as threesome components: OLM, AML, and HCT (combination I) and AML, VAL, and HCT (combination II). The separation was achieved by using an RP-CN column, and acetonitrile-methanol-10 mmol orthophosphoric acid pH 2.5 (7 : 13 : 80, v/v/v) was used as a mobile phase; the detector wavelength was set at 235 nm. The linear ranges were found as 0.1-18.5  μ g/mL, 0.4-25.6  μ g/mL, 0.3-15.5  μ g/mL, and 0.3-22  μ g/mL for AML, OLM, VAL, and HCT, respectively. In order to check the selectivity of the method for pharmaceutical preparations, forced degradation studies were carried out. According to the validation studies, the developed method was found to be reproducible and accurate as shown by RSD ≤6.1%, 5.7%, 6.9%, and 4.6% and relative mean error (RME) ≤10.6%, 5.8%, 6.5%, and 6.8% for AML, OLM, VAL, and HCT, respectively. Consequently, the method was applied to the analysis of tablets and plasma of the patients using drugs including those substances.

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In this paper, a molecularly imprinted polymer (MIP) coating grafted to a trimethylolpropane trimethacrylate (TRIM) core material for CEC was reported. The core monolith was prepared with a solution of 20% (w/w) TRIM in a mixture of porogen and a polymerization precursor, which can generate a stable electroosmotic flow due to the formation of ionizable groups after postpolymerization hydrolization. Graft polymerization took place on the resultant TRIM monolith with a mixture of template, methacrylic acid, and ethylene glycol dimethacrylate. Strong recognition ability (selectivity factor was 5.83) for S-amlodipine and resolution of enatiomers separation (up to 7.99) were obtained on the resulting grafted imprinted monolith in CEC mode. The influence of CEC conditions on chiral separation, including the composition of mobile phase, pH value, and the operating voltages was studied. These results suggest that the method of grafted polymerization reported here allows a rapid development of MIP monolith once core materials with desired properties are available, and is a good alternative to prepare CEC-based monolithic MIPs.

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To compare 24-hour blood pressure control and adverse effects in patients with essential hypertension who were switched from amlodipine to nisoldipine.

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Data from 12,265 patients treated with amlodipine/valsartan from three studies were analyzed in a meta-analysis. These studies focused on (i) non-diabetic hypertensive patients suffering from abdominal obesity; (ii) hypertensive patients with at least one metabolic risk factor; and (iii) hypertensive patients with type 2 diabetes mellitus. The observation periods were 16 weeks for the first two and 24 weeks for the latter cohort.

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With the aim to determine the influence of reducing systolic blood pressure in urinary TGF-beta1 of type 2 diabetes (DM2) with diabetic nephropathy (DN), 21 subjects with type 2 diabetes and proteinuria >500 mg/24 h were studied. Amlodipine and ramipril were added to their previous antihypertensive treatment for 12 weeks. Urinary TGF-beta1 (UTGF-beta1) was determined at 0, 4, 8 and 12 weeks. Plasma TGF-beta1 was determined at 0 and 12 weeks. Subjects whose mean systolic blood pressure (SBP) during treatment were under 140 mmHg were grouped as the better SBP controlled group (n = 11) and those with SBP equal to or greater than 140 mHg were grouped in a moderate SBP controlled group (n = 10). Compared to baseline, mean log UTGF-beta1 at 4, 8 and 12 weeks decreased (-0.22 +/- 0.15 pg/mg; p = 0.04) in better SBP controlled group but not in the moderate SBP controlled group (-0.12 +/- 0.08 pg/mg, p = 0.82). Mean SBP correlated with UTGF-beta1 (r = 0.458, p = 0.0357), and this effect was independent of HbA1c (p = 0.042). By controlling SBP in DM2 subjects with DN we might decrease UTGF-beta1. We propose that reduction of UTGF-beta1 is due to a decrease in renal TGF-beta1 production.

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Prospective, randomized, open, blinded endpoint trial with a double-blinded 2 x 2 factorial component.

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Endothelial production of nitric oxide (NO) is attenuated in patients with essential hypertension. We investigated whether treatment with amlodipine increased exhaled NO output (VNO) at rest and during exercise in patients with essential hypertension.

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Grapefruit juice has no appreciable effect on amlodipine pharmacodynamics or pharmacokinetics, including its stereoselective kinetics. Bioavailability enhancement by grapefruit juice, noted with other dihydropyridine calcium antagonists, does not occur with amlodipine. Once daily grapefruit juice administration with usual oral doses of amlodipine is unlikely to alter the profile of response in clinical practice.

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Rats intravenously catheterized for blood collection were randomly divided into groups that were administered the vehicle, the ARB valsartan or valsartan combined with one of the 2 CCBs. Their blood and kidneys were collected 270 min after administration.

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norvasc 10 mg 30 tablet 2017-07-23

Bilateral upper extremity edema has been associated with amlodipine use Diovan Brand in a child with an abnormal arterial circulation. The edema resolved upon discontinuation of the drug.

norvasc dosage information 2016-09-28

This observational study evaluated the efficacy and tolerability of 3-month aliskiren Menosan Capsules /amlodipine therapy under outpatient conditions.

norvasc 5 mg twice daily 2016-12-23

1. Voltage-operated calcium channel (VOCC) antagonists are effective antihypertensive and antianginal agents but they also depress myocardial contractility. 2. We compared four L-type calcium channel antagonists, felodipine, nifedipine, amlodipine and verapamil and a relatively T-type selective calcium channel antagonist, mibefradil, on human and rat isolated tissue assays to determine their functional vascular to cardiac tissue selectivity (V/C) ratio. 3. The V/C ratio was calculated as the ratio of the IC50 value of the antagonist that reduced (by 50%) submaximally contracted (K+ 62 mM) human small arteries from the aortic vasa vasorum (vascular, V) mounted in a myograph and the IC50 value of the antagonist that reduced (-)-isoprenaline (6 nM) submaximally stimulated human right atrial trabeculae muscle (cardiac, C) mounted in organ chambers. 4. The average pIC50 values (-log IC50 M) for the human vascular preparations were felodipine 8.30, nifedipine 7.78, amlodipine 6.64, verapamil 6.26 and mibefradil 6.22. The average pIC50 values for the cardiac muscle were felodipine 7.21, nifedipine 6.95, verapamil 6.91, amlodipine 5.94, and mibefradil 4.61. 5. The V/C ratio calculated as antilog [pIC50V-pIC50C] is thus mibefradil 41, felodipine 12, nifedipine 7, amlodipine 5 and verapamil 0.2. 6. In rat small mesenteric arteries the pIC50 values for the five drugs were similar to the values for human vasa vasorum arteries contracted by K+ 62 mM. However for methoxamine (10 microM) contraction in the rat arteries the Pamelor Maximum Dose pIC50 values were lower for felodipine 7.24 and nifedipine 6.23, but similar for verapamil 6.13, amlodipine 6.28 and mibefradil 5.91. 7. In conclusion. in the human tissue assays, the putative T-channel antagonist mibefradil shows the highest vascular to cardiac selectivity ratio; some 3 fold higher than the dihydropyridine, felodipine, and some 200 fold more vascular selective than the phenylalkylamine, verapamil. This favourable vascular to cardiac selectivity for mibefradil, from a new chemical class of VOCC antagonist, may be explained by its putative T-channel selectivity.

norvasc side effects reviews 2016-03-29

Randomized patients, (n = 524) including 128 patients with isolated systolic hypertension (ISH); mean age: 72.4 years; mean systolic/ Zithromax Dose Pediatric Pneumonia diastolic blood pressures (SBP/DBP): 174.5/97.9 mmHg.

norvasc dose 2016-06-30

After confirming hypertension in the absence of antihypertensive treatment, blood pressure control was achieved by administration of amlodipine at individually adjusted doses. Hormone replacement therapy (HRT) was introduced in a cyclic Exelon 3 0 Mg Hartkapseln regimen (21 of 28 days) with percutaneous estradiol (1.5 mg/day) and vaginal micronized progesterone (100 mg/day).

norvasc generic name amlodipine 2015-09-06

The effects of amlodipine (0.3 mg/kg administered intravenously, n = 5) and placebo (n = 5) on recovery of myocardial function and respiration of isolated mitochondria were examined in "stunned" myocardium of normotensive pentobarbital-anesthetized dogs. Measures of myocardial wall motion, using sonomicrometers, and tissue blood flow, by radioactive microspheres, were obtained at baseline, 15 minutes after administration of amlodipine or placebo, after 10 minutes of left circumflex artery ligation and at 60 minutes of reperfusion. Mean aortic pressure decreased from 115 +/- 6 to 101 +/- 5 mm Hg after administration of amlodipine and remained decreased throughout the experiment. Heart rate was not significantly affected at any time. Both groups showed similar degrees of ischemia: elevation of ST segment to 4.7 +/- 1.4 vs 6.2 +/- 1.9 mV; reduction of ischemic zone shortening fraction to 0.6 +/- 1.9 vs -3.4 +/- 2.7%; and reduction of epicardial and endocardial blood flows (epicardial = 40 +/- 13 vs 43 +/- 13 ml/100 g/min; endocardial = 7 +/- 4 vs 13 +/- 6 ml/100 g/min [values for amlodipine vs placebo]). Mitochondrial state 3 rate of respiration and respiratory control index indicative of rate of adenosine triphosphate synthesis and Celexa 20 Mg Pill Identification membrane integrity in myocardial samples taken after 10 minutes of ischemia were significantly reduced in the placebo but not in the amlodipine group. Myocardial function showed significantly greater improvement in amlodipine vs placebo at 60 minutes of reperfusion as indicated by shortening fraction (17.7 +/- -1.4 vs 5.8 +/- -3.5%, amlodipine vs placebo), which may have been related to increased myocardial blood flow and decreased blood pressure during reperfusion. Thus, amlodipine pretreatment prevented mitochondrial dysfunction during ischemia and accelerated recovery of both myocardial mechanical function and blood flow when compared with placebo.

norvasc 5 mg 2015-03-28

Thirty-four young hypertensives ( Cordarone 150 Mg age 28-55, median 47) rotated in a double-blind, Latin-square, crossover fashion through 6 weeks of treatment each with amlodipine, doxazosin, lisinopril, bisoprolol, bendrofluazide and placebo. Blood pressure was measured at each visit. 'Best' drug, defined by efficacy and tolerability, was repeated at the end.

norvasc generic reviews 2016-12-09

Activation of VSMC Ca2+ channels and CaMKII is a key early signaling event required for Alprostadil 300 Mg upregulation of PCNA gene expression in VSMCs after oxidative injury to endothelium.

30 mg norvasc too much 2016-04-04

In 6,775 evaluable hypertensive patients distributed over the 17 Spanish autonomous communities (ACs), the 10-year risk of experiencing a coronary event (CR) was calculated using the Framingham equation, while risk of coronary death (RCD) and vascular death (RVD) was calculated using the Score project system, both at baseline and after one year of blood pressure control with amlodipine at the required dose. A comparison was made of the capacity to detect risk differences by both methods between populations with known different risks, and in the same population as a result Is Arava A Biologic Drug of blood pressure control.

norvasc reviews by patients 2015-02-26

Hypertensive patients whose blood pressures are more than 20 mmHg above their goal will often require three or more medications. Careful selection of medications whose actions are complementary or have an improved adverse effect profile when combined can affect not only the blood pressure but also patient acceptance, thus improving persistence in taking the medications as prescribed. This review will highlight the three single-pill three-drug combinations currently available in the US and will address their efficacy, safety, and tolerability. All three include the dihydropyridine calcium-channel blocker, amlodipine, and the thiazide diuretic, hydrochlorothiazide. They each contain a different renin-angiotensin system blocker. One includes the angiotensin-receptor blocker, olmesartan, while another contains valsartan. The third combination includes the Claritin Sinus Medicine direct renin inhibitor, aliskiren. All three fixed-dose combinations (FDC) at maximum doses of each component lowers the blood pressure of patients with stage II hypertension by 37 to 40 mmHg systolic and 21 to 25 mmHg diastolic, which is superior to any two of the components that comprise the three-drug FDC. These drugs are effective in males and females, the elderly, diabetics, minority populations, and patients with metabolic syndrome. Triple-drug FDCs are well tolerated with a low incidence of adverse effects, the most common being peripheral edema related to amlodipine. Extrapolation of data from two-drug FDC suggests that medication compliance (adherence and persistence) should be better with these FDCs than with the individual components taken as separate medications, although additional studies are necessary to confirm this.