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Norvasc (Amlodipine)
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Norvasc

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:

Similar Products:
Norvasc, Plendil, DynaCirk, Catdene, Procardia, Adalat

 

Also known as:  Amlodipine.

Description

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.

Dosage

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.

Overdose

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.

Storage

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.

Contraindications

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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Several studies have shown the benefits of antihypertensive treatment in elderly patients in terms of cardiovascular morbidity and mortality rate reduction. Low-dose drug combinations may be of interest in treating older subjects. A randomized, multicenter, double-blind, parallel group study was conducted to compare the efficacy and safety of bisoprolol 2.5 mg/hydrochlorothiazide 6.25 mg (n = 84) to amlodipine 5 mg (n = 80) in isolated systolic hypertension in patients older than 60 years.

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Chronic heart failure (CHF) has high morbidity and mortality rates despite treatment with angiotensin-converting enzyme inhibitors, diuretics, and digoxin. Adjunctive vasodilation through calcium channel blockade has been suggested as potentially useful. However, the first-generation calcium channel blockers, including the dihydropyridine nifedipine, showed disappointing results in CHF. The second-generation dihydropyridines were expected to be of more value, and of all the calcium channel blockers, these drugs were the ones most studied in patients with CHF.

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Losartan alone decreased SAP and DAP from 150 ± 11/91 ± 7 to 132 ± 12/81 ± 8 mm Hg (office measurement) and from 144 ± 10/86 ± 9 to 128 ± 12/76 ± 10 mm Hg (24-hr monitoring); heart rate decreased fom 74 ± 8 to 70 ± 8/min (p < 0.05). SAP and DAP in 66 patients who completed stage 2 was 122 ± 6/73 ± 6 mm Hg or significantly lower than before therapy (147 ± 9/87 ± 9) (p < 0.001). Mean daily decrease of SAP and DAP according to 24-hr monitoring decreased from 144 ± 10 to 128 ± 12 and from 86 ± 9 to 76 ± 10 mm Hg respectively (p < 0.001). The target AP value was reached in 73% of the cases (99 out of 136 patients) after stage 1 and in 95% cases (63 out of 66) after stage 2. The values of LVMI (105 ± 23 and 98 ± 26 g/m2), PWPR from 16 ± 2.1 to 13 ± 3.5 m/s (p < 0.05), IMT (0.76 ± 0.16 and 0.80 ± 42 mm), and microalbuminuria (11.0 ± 1.7 and 8.6 ± 0.7 mg/24 hr) before and after completion of stage 2 were not significantly different in 66 patients (p > 0.05). Biochemical parameters of blood did not appreciably change. The safety profiles of both drugs were on the whole positive. Deaths and adverse reactions were absent barring clinically insignificant side effects in 28 of the 160 patients (17.5%).

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Of 4146 patients prescribed the AA single pill, 11% failed to fill the first repeat prescription and 33% had ceased treatment by 12 months (MPT, 35 months). Of 6204 patients prescribed amlodipine and atorvastatin as two pills, 23% failed to fill the first repeat prescriptions and 59% had ceased treatment by 12 months (MPT, 7 months). In a multivariate model, cessation of single-pill therapy increased by 165% if there was no prior therapy, but only increased by 48%-55% if there was no prior therapy with a calcium channel blocker or statin. MPT on the single pill was 8 months in those without prior antihypertensive therapy, but was ≥ 37 months in those with any prior antihypertensive therapy.

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Hydrate formation and dehydration phenomena are frequently encountered phase transformations during manufacturing and storage of the drug products. It is essential to understand, monitor, and control these transformations to ensure that the quality attributes of the drug product are not affected. In this work, phase transformations of the solid forms of amlodipine besylate (AMB) were studied using Raman and near-infrared (NIR) spectroscopy. AMB exists as anhydrate (AH), monohydrate (MH), dihydrate (DH), and amorphous (AM) form. Solid form quantification models based on multivariate data analysis of the Raman and NIR spectra were developed. The AH, MH, and AM form were transformed to the DH during solubility measurements. The AH to DH transformation also occurred during wet granulation. The transformation kinetics were faster during wet granulation than during the solubility experiments. This was due to the shear forces involved in granulation that can facilitate nucleation and can enhance the overall transformation. The DH form present in the wet granules persisted after drying, and final granules contained a mixture of the AH and DH. The relative importance of the dissolution, nucleation, and growth steps for the transformation was elucidated using optical microscopy experiments. The transformation kinetics were found to be limited by nucleation and growth.

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Six impurities ranging from 0.43 to 1.42% in amlodipine maleate were detected by a simple isocratic reverse-phase high performance liquid chromatography (HPLC). LC-MS was performed to identify the mass of the impurities. Based on the spectral data (IR, NMR and MS), the structures of these impurities were characterized as 3-ethyl 5-methyl 4-(2-chlorophenyl)-2-[2-(1,3-dioxo-2,3-dihydro-1H-2-isoindolyl)ethoxymethyl]-6-methyl-1,4-dihydro-3,5-pyridinedicarboxylate (impurity I); 5-ethyl 3-methyl 4-(2-chlorophenyl)-2-methyl-6-[2-(2-methylcarbamoylphenyl-carboxamido)ethoxymethyl]-1,4-dihydro-3,5-pyridinedicarboxylate (impurity II); besylate salt of 3-ethyl 5-methyl 2-(2-aminoethoxymethyl)-4-(2-chlorophenyl)-6-methyl-3,5-pyridinedicarboxylate (impurity III); dimethyl 2-(2-aminoethoxymethyl)-4-(2-chlorophenyl)-6-methyl-1,4-dihydro-3,5-pyridinecarboxylate (impurity IV); 3-ethyl 5-methyl 2-(2-aminoethoxymethyl)-4-(4-chlorophenyl)-6-methyl-1,4-dihydro-3,5-pyridinedicarboxylate (impurity V); diethyl 2-(2-aminoethoxymethyl)-4-(2-chlorophenyl)-6-methyl-1,4-dihydro-3,5-pyridinedicarboxylate (impurity VI).

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The forearm blood flow (FBF) was measured in 25 patients with essential hypertension and in 25 normotensive subjects by using strain-gauge plethysmography during reactive hyperemia (RH) (280 mm Hg for 5 min) and after sublingual administration of nitroglycerin (NTG, 0.3 mg).

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Hypertension is a common problem in elderly cats. In most cats, systolic blood pressure (SBP) of <160 mmHg is achieved in response to amlodipine besylate at either 0.625 or 1.25 mg q24h. The individual cat factors determining dose requirement dose have not been explored.

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Eighty subjects with type 2 diabetic nephropathy were randomly divided into two groups: losarten group (n = 41) and amlodipine group (n = 39). Fasting blood was drawn to determine HbA1c, insulin and adiponectin levels. Insulin resistance was calculated using fasting glucose and insulin, expressed as HOMA-IR. For assessment of the relationship between adiponectin and other parameters, Pearson sample correlation coefficients were used. After stratification, ARB losartan (100 mg daily) was administered for a period of 6 months.

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A Prospective observational study was carried out for the period of six months in an out-patient department. Elderly patients who have been diagnosed with hypertension as per JNC-7 guidelines and patients receiving or prescribed with antihypertensive drugs were included.

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Comparable BP reductions were obtained. UAE at endpoints ware as follows (mg/gCr, *P<0.01): nifedipine CR 30.8 (17.3-81.1),* cilnidipine 33.9 (18.0-67.7),* efonidipine 51.0 (21.2-129.8), amlodipine 40.6 (18.7-94.7). By all agents, significant augmentations were observed in PRA, angiotensin I and angiotensin II (AngII). AngII at cilnidipine was significantly lower than that at amlodipine. PAC at cilnidipine and efonidipine was significantly lower than that at amlodipine. Nifedipine CR significantly reduced ANP concentration.

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By following JNC guidelines, a slightly higher percentage of patients will achieve hypertension control with a newer class calcium channel blocker (amlodipine) but at a substantially higher cost than with a generic diuretic (chlorthalidone).

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We compared effects of racemic amlodipine and S-amlodipine in 127 patients with 1-2 degree arterial hypertension (AH) on structural-functional parameters of the left ventricle and brachial artery as well as on characteristics of carbohydrate, lipid, electrolyte, and purine metabolism. Racemic amlodipine was given to 66 and S-amlodipine--to 61 patients. Duration of therapy was 24 weeks. In all patients we observed positive and comparable hypotensive effect while doses of S-amlodipine were significantly lower than those of racemic amlodipine (7.5 +/- 0.8 and 11.6 +/- 1.4 mg/day, respectively, p < 0.01). Monotherapy with S-amlodipine resulted in complete regression of left ventricular hypertrophy in 55% and normalization of left ventricular diastolic function in 62.4% of cases; significant improvement of brachial artery vasomotor function was also observed. In addition treatment with S-amlodipine for 24 weeks in patients with hyperlipidemia led to significant lowering of levels of atherogenic lipoproteins and total cholesterol.

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Based on the review and recommendation of the American Diabetes Association's Subcommittee on Ethical Scientific Publications (ESP), Diabetes Care formally retracts the above-cited article. For reasons described below, the published data are considered to be unreliable. According to an investigation and analysis of the data conducted by Shiga University of Medical Science (report received 25 November 2013), 10.1% of the albumin-to-creatinine ratio (ACR) data reported in the article did not match original patient records. In the valsartan and amlodipine groups, respectively, 12.5% and 8.1% of the ACR data reported in the article differed from patient records. Close examination of these differences showed that ACR values reported for the valsartan group were smaller, and those for the amlodipine group were larger, than values reported in patient records; these differences "worked to the advantage of valsartan." The investigative panel of Shiga University of Medical Science concluded that the above-cited article is "inappropriate for [a] scientific paper."

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By the end of BPLA in both groups originally assigned statin or placebo, approximately 65% were receiving a statin, and lipid levels had equalized. The benefits of atorvastatin observed in LLA were sustained throughout BPLA. At the end of BPLA, in those assigned amlodipine-based therapy, atorvastatin reduced coronary heart disease deaths and nonfatal myocardial infarction (MI) by 46% [hazard ratio 0.54, confidence interval (CI) 0.40-0.72, P < 0.0001], stroke by 37% [hazard ratio 0.63, CI 0.46-0.87, P = 0.004] and total cardiovascular events and procedures by 27% [hazard ratio 0.73, CI 0.63-0.86, P < 0.0001]. In the atenolol-based group, atorvastatin reduced coronary heart disease death and nonfatal MI by 25% [hazard ratio 0.75, CI 0.57-0.97, P = 0.03], stroke by 10% [hazard ratio 0.90, CI 0.69-1.18, P = 0.43] and total cardiovascular events and procedures by 13% [hazard ratio 0.87, CI 0.76-1.0, P = 0.05]. P values for heterogeneity were low, but failed to achieve statistical significance (0.10, 0.10 and 0.11 for chronic heart disease, stroke and total cardiovascular events, respectively).

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Valsartan addition to dual therapy with amlodipine + HCTZ was more effective than ramipril addition in reducing LVH.

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To assess quality of life (QoL) in unselected patients in primary care treated with a fixed-dose combination of olmesartan and amlodipine. Research design and methods. Multicenter, noninterventional, noncontrolled observational study in 8241 patients seen by 2187 physicians over 12 - 18 weeks.

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Angiotensin II can influence adipocytokine levels in adipose tissue, but the association between aldosterone, which mediates the effect of angiotensin II, and adipocytokines has yet to be fully elucidated. This study was designed to investigate the effect of spironolactone, a representative aldosterone blocker, on adipocytokines such as adiponectin, visfatin, plasminogen activator inhibitor (PAI)-1 and tumor necrosis factor alpha in patients with type 2 diabetic nephropathy: the study included 33 patients, 22 of whom were randomly assigned to the spironolactone (50 mg/d) group and 11 to the amlodipine (2.5 mg/d) group. Data were collected at baseline and after 3 months of treatment and compared with baseline data for 25 age-matched healthy subjects. A significant decrease in plasminogen activator inhibitor 1 in the spironolactone group was observed (22.6 +/- 13.4 to 19.2 +/- 11.3 ng/mL, P =.0323), but this did not occur in the amlodipine group. Adiponectin and visfatin levels did not change in the spironolactone and amlodipine groups, but significant increases in these adipocytokines were found in a subgroup of patients in the spironolactone group with glycated hemoglobin A(1c) (HbA(1c)) 8.0% or greater (11.8 +/- 6.4 to 13.3 +/- 7.4 microg/mL, P = .0344; and 1.39 +/- 0.92 to 2.26 +/- 0.76 ng/mL, P =.0397, respectively). The tumor necrosis factor alpha level at baseline exceeded the lower detection limit of the assay in only 6 patients in the spironolactone group, and no change occurred in these patients. Moreover, neither spironolactone nor amlodipine therapy caused a change in high-sensitivity C-reactive protein or soluble CD40 ligand, but a significant decrease in the level of brain natriuretic peptide was found in the spironolactone group only. Furthermore, significant increases of HbA(1c), creatinine, potassium, and aldosterone levels and plasma renin activity, and a decrease in urinary albumin excretion were also observed only in the spironolactone group. The number of patients with HbA(1c) 8.0% or greater increased after spironolactone treatment. A significant decrease in systolic but not in diastolic blood pressure was observed in both treatment groups. In conclusion, our data suggest that in patients with type 2 diabetes mellitus complicated by diabetic nephropathy, spironolactone can decrease plasminogen activator inhibitor 1 and brain natriuretic peptide levels in addition to urinary albumin excretion, and systolic blood pressure, and that in patients with poor glycemic control, spironolactone can increase the levels of adiponectin and visfatin. However, the significant elevation of HbA(1c) levels by spironolactone should be emphasized.

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There were no significant differences in BP and tolerability between the three groups. The percentage changes in UPCR at 12 months after start of the combination therapy were significantly different in the HCTZ group (-26.3 ± 11.1 %, mean ± SE) and CCB group (+46.7 ± 33.6 %, p < 0.05), while eGFR was significantly lower in the HCTZ group than in the ACEI group or CCB group at 4 months but not at 12 months.

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The Medline databank was used to search studies in human beings (published in 1990 or later) that used dihydropyridines in patients with CHF. The references of the studies found were subsequently checked for additional data. In 17 studies and more than 2000 patients with CHF, no consistent beneficial effect was observed with regard to exercise tolerance and functional capacity, whereas plasma neurohormones were not affected. On the other hand, in general, no worsening of CHF was seen with these second-generation dihydropyridines. Two larger studies (PRAISE and V-HeFT III) have given some estimates on the long-term effects of dihydropyridines, and no overall influence on mortality rate was found. Of note, subanalysis of the PRAISE study has suggested that in patients with a nonischemic cause of CHF, amlodipine might have a beneficial effect on survival.

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The specific activities for human CYP isoforms included 7-ethoxyresorfin O-deethylation (CYP1A1), phenacetin O-deethylation (CYP1A2), coumarin 7-hydroxylation (CYP2A6), 7-benzyloxyresorufin O-dealkylation (CYP2B6), S-warfarin 7-hydroxylation (CYP2C9), S-mephenytoin 4'-hydroxylaion (CYP2C19), bufuralol 1'-hydroxylation (CYP2D6), chlorzoxazone 6-hydroxylation (CYP2E1), and testosterone 6beta-hydroxylation (CYP3A4). Benidipine and amlodipine competitively inhibited the CYP1A1 activity. Nifedipine, nisoldipine and aranidipine competitively inhibited the CYP1A2 activity. No 1,4-dihydropyridie calcium antagonists used in this study inhibited the CYP2A6 activity. Barnidipine and amlodipine inhibited the CYP2B6 activity. Nicardipine, benidipine, manidipine and barnidipine competitively inhibited the CYP2C9 and CYP2D6 activities. Inhibition extent of the CYP2E1 activity by nifedipine and aranidipine were weak. Nicardipine, benidipine and barnidipine inhibited the CYP2C19 and CYP3A4 activities. Among the human CYP isoforms investigated, the inhibitory effects of 1,4-dihydropyridine calcium antagonists were potent on human CYP1A2, CYP2B6, CYP2C9, CYP2C19 and CYP2D6 as well as CYP3A4. Furthermore, the isoform selectivity of inhibition by 1,4-dihydropyridine calcium antagonists was clarified.

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In all categories CCBs were the third commonly prescribed antihypertensive as monotherapy, with a prescription rate of 11.1% in uncomplicated hypertension, 18% in diabetic hypertension and 20.1% in elderly patients above 65 years of age. Nifedipine formulations were the most extensively prescribed CCBs. Almost half of the CCB-treated patients were on IR-nifedipine, whereas IR-diltiazem and IR-verapamil, and amlodipine were infrequently prescribed.

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To evaluate the anti hypertensive efficacy and tolerability of amlodipine given once daily either morning and evening doses.

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In this study, we will investigate the improvement of coronary plaque with IVUS by treatment with two dihydropyridine CCBs in hypertensive patients undergoing elective PCI. This result will lead to the discovery of more effective drug therapy for inhibition of coronary events.

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Telmisartan is an angiotensin II receptor blocker, which acts as a partial agonist of peroxisome proliferator activator receptor-γ (PPAR-γ). Because PPAR-γ initiates a variety of antiinflammatory responses, the effect on myocardial ischemia is to be elucidated.

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We compared the effects of three dihydropyridine calcium antagonists (felodipine, nifedipine and amlodipine) on left ventricular (LV) contractile performance and diastolic filling dynamics in eight conscious animals. After administering metoprolol and atropine, felodipine (25 nmol/kg i.v.) produced significant decreases in LV end-systolic pressure (PES) (109 +/- 15 vs. 88 +/- 12 mmHg, P < .05) and arterial elastance (Ea) (12.6 +/- 4.5 vs. 8.5 +/- 3.4 mmHg/ml, P < .05), whereas the heart rate was unchanged. Felodipine increased the slopes of the end-systolic P-V relation (7.4 +/- 0.9 vs. 9.9 +/- 1.0 mmHg/ml, P < .05), the dP/dtmax-end diastolic volume (VED) relation (68.1 +/- 11.2 vs. 94.9 +/- 14.3 mmHg/sec/ml, P < .05), and the stroke work (SW)-VED relation (72.1 +/- 3.1 vs. 82.8 +/- 5.2 mmHg, P < .05), and shifted all three relations to the left, indicating enhanced contractile performance. In contrast, at doses that produced equivalent reductions of PES, nifedipine (375 nmol/kg i.v.) and amlodipine (780 nmol/kg i.v.), significantly decreased the slopes of the end-systolic P-V relation, the dP/dtmax-VED relation and the SW-VED relation and shifted all three relations to the right, indicating depressed LV contractile performance. Felodipine decreased the time constant (T) of LV relaxation (32.2 +/- 5.2 to 28.8 +/- 5.2 msec, P < .05) and increased the maximum rate of early diastolic LV filling (dV/dtmax) (167 +/- 22 to 207 +/- 26 ml/sec, P < .05). Amlodipine had the opposite effect, slowing T (31.0 +/- 4.9 to 33.9 +/- 5.4 msec, P < .05) and decreasing dV/dtmax (173 +/- 39 to 154 +/- 30 ml/sec, P < .05), whereas nifedipine had no significant effects on T, PGmax or dV/dtmax. Thus, we conclude that in conscious dogs after autonomic blockade, at dosages that produced equivalent arterial vasodilation, felodipine augmented, whereas amlodipine depressed, LV contractile performance, LV relaxation and early LV filling. Nifedipine decreased LV contractile performance but had no significant effect on LV relaxation and early LV filling.

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These results suggest that azelnidipine induces long-lasting vascular relaxation by inhibiting voltage-dependent L-type Ca2+ channels in vascular smooth muscle.

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Combination therapies with angiotensin II type I receptor blockers (ARBs) and calcium channel blockers (CCBs) are frequently administered to hypertensive patients, because these regimens have renoprotective and antihypertensive effects. However, few studies have focused on the renoprotective effects of individual CCBs when combined with ARBs for hypertension.

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Medical records from cats with systemic hypertension and hypertensive retinopathy were reviewed.

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norvasc generic image 2016-10-12

Based on the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack (ALLHAT) Trial, the Seventh Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC-7) states that "thiazide-type diuretics should be used as initial therapy for most patients with hypertension." In the ALLHAT buy norvasc study, although there was no difference in the primary outcome for fatal heart attack and nonfatal myocardial infarction between all treatment groups, the manuscript endorses thiazide-type diuretics as first choice, based on their cardioprotective effects and low cost. It is well known that thiazide-type diuretics cause hypokalemia, glucose intolerance, and diabetes, although the ALLHAT study showed a significant 43% to 65% higher risk of new-onset diabetes with chlorthalidone compared with amlodipine (30%) and lisinopril (18%). The investigators justified the fact that the greater incidence of diabetes did not translate into more cardiovascular events. Such a conclusion ignores that the morbidity and mortality from diabetes manifests over decades and not the mere 2- to 6-year time frame examined in the ALLHAT study. It would appear that the strong endorsement of thiazide-type diuretics as first-line therapy by the JNC-7 will lead to a higher incidence of diabetes in these patients.

norvasc overdose symptoms 2016-02-26

Despite the well documented benefits conferred by adequate control of hypertension, the majority of buy norvasc hypertensive patients display suboptimal control and few patients achieve blood pressure (BP) levels <140/90 mmHg. As a consequence, combination therapy will be required in the majority of patients to achieve target BP. Fixed-dose combinations of antihypertensives not only simplify treatment regimens, contributing to enhanced patient adherence, they provide superior BP-lowering efficacy and an improved tolerability profile. Fixed-dose combinations have become the strategy of choice in high-risk patients or those with stage 2-3 hypertension. The combination of a renin-angiotensin system inhibitor (RASI) with a calcium channel blocker (CCB) is a first-line combination that, in addition to its antihypertensive efficacy, reduces oedema, the main adverse effect of the dihydropyridine CCB and the main factor limiting their use. In morbidity/mortality studies, this fixed-dose combination has also demonstrated superiority over a RASI combined with a diuretic. The single-pill combination of telmisartan and amlodipine has been shown to produce a dose-dependent BP-lowering effect significantly greater than that of either agent administered as monotherapy. These findings have been confirmed by ambulatory BP monitoring in patients with stage 1 and 2 hypertension, which demonstrated that single-pill telmisartan/amlodipine provides substantial 24-hour BP-lowering efficacy. A higher proportion of patients achieved 24-hour BP goals of <130/80 mm Hg on combination therapy. The superior efficacy of combination therapy has been demonstrated across a broad range of patients, including those with moderate-to-severe hypertension, diabetes mellitus and obesity. Moreover, combined use of telmisartan and amlodipine reduces the incidence of amlodipine-induced oedema, making it a preferred combination for the treatment of hypertension.

norvasc 5 mg 2015-03-10

A rapid, precise, sensitive, economical, and validated high performance thin layer chromatographic method is developed for simultaneous quantification of olmesartan medoxomil and hydrochlorothiazide in combined tablet dosage form. The method used amlodipine as internal standard (IS). Chromatographic separations were achieved on silica gel 60 F254 plates using toluene-methanol-ethyl acetate-acetone (2.5 : 1 : 0.5 : 2, v/v/v/v) as mobile phase. Densitometric analysis was carried out in the reflectance mode at 258 nm. Calibration curves were linear over a range of 80-480 ng/band for olmesartan medoxomil and 25-150 ng/band for hydrochlorothiazide. The detection and quantification limits were found to be 18.12 and 56.35 ng/band for olmesartan medoxomil and 6.31 and 18.56 ng/band for hydrochlorothiazide, respectively. Intra- and interassay precision provided relative standard deviations lower than 2% for both analytes. Recovery from 99.60 to 101.22% for olmesartan medoxomil and 98.30 to 99.32% for hydrochlorothiazide show good accuracy. Both the drugs were also subjected to acid, alkali, oxidation, heat, and photodegradation studies. The degradation products obtained were well resolved from pure drugs with significantly different R f values. As the method could effectively separate the drugs from their degradation products, it buy norvasc can be used for stability-indicating analysis. Validation of the method was carried out as per international conference on harmonization (ICH) guidelines.

norvasc tablet benefits 2015-10-31

On average, the systolic and diastolic blood pressures were reduced from 161 ± 14 to 135 ± 10 mmHg and 93 ± 9 to 81 ± 6 mmHg, respectively. Blood pressure values of < 140/90 mmHg and < 130/80 mmHg were achieved in 56 and 7 % patients, respectively. A subgroup analysis of 242 patients (43 %) with diabetes mellitus and/or renal disease, as well as those with a high cardiovascular risk, demonstrated nearly identical results compared to the total population. Overall, 44 adverse events were documented in 41 patients, and buy norvasc physicians reported that 94 % of patients were compliant in a final survey on evaluation of therapy.

norvasc medication 2015-02-19

One hundred ninety-two hypertensive patients across 10 study centers were randomly assigned to double-blind monotherapy with amlodipine besylate buy norvasc (5 mg/d), nifedipine CC (30 mg/d), or nifedipine GITS (30 mg/d) for 8 weeks. Patients not achieving therapeutic response after 4 weeks had their dose doubled for the next 4 weeks. The primary end point was a comparison of the average reduction (week 8 minus baseline) in 24-hour ambulatory diastolic blood pressure (DBP). Secondary end points included a comparison of average 24-hour ambulatory systolic blood pressure (SBP), office SBP or DBP reduction, responder rates, safety, and tolerability.

norvasc dosing information 2017-01-03

Calcium channel blocker poisonings account for a substantial number of reported deaths from cardiovascular drugs. Although supportive care is the mainstay of treatment, experimental therapies such as high-dose insulin-euglycemia and lipid emulsion have been studied in animal models and used in humans. In the most severe cases, even aggressive care is inadequate and deaths occur. In both experimental models and clinical cases of vasodilatory shock, methylene blue improves hemodynamic measures. It acts as a nitric oxide scavenger and inhibits guanylate cyclase that is responsible for the production of cyclic guanosine monophosphate (cGMP). Excessive cGMP production is associated with refractory vasodilatory shock in sepsis and anaphylaxis. The aim of this study is to determine the efficacy of methylene blue buy norvasc in an animal model of amlodipine-induced shock.

norvasc dosage strengths 2017-09-13

European guidelines recommend a combination of at least two antihypertensive drugs to achieve blood pressure (BP) goals in the majority of patients. In addition, they encourage simplification of treatment regimens using single-pill, fixed-dose combinations (FDCs) to aid compliance. Of the preferred combinations, those based on angiotensin II receptor blockers (ARBs) may be more desirable than those based on angiotensin-converting enzyme inhibitors, because of equivalent efficacy and superior tolerability. Significantly better BP reductions and control rates have been observed with the dual combinations of ARBs with amlodipine or hydrochlorothiazide (HCZT) compared with component monotherapies. Furthermore, in the 15-20% of patients who require triple combination therapy to achieve BP goals, fixed-dose triple combinations with an ARB, calcium-channel blocker and diuretic, which have recently become available, provide significantly better BP reductions and control compared with dual combinations. Within the ARB class, olmesartan stands out buy norvasc as being one that has been recently investigated in a considerable number of studies that are relevant to the modern concept of FDC therapy in terms of both dual and triple combination therapy. The availability of such single-pill FDCs has the potential to deliver strong antihypertensive efficacy with good tolerability and improved compliance.

norvasc positive reviews 2017-12-01

A rapid and sensitive liquid chromatography-tandem mass spectrometry (LC-MS/MS) method has been developed and validated for the buy norvasc estimation of amlodipine in human plasma. Amlodipine was extracted from human plasma by using a solid-phase extraction technique. Imipramine was used as the internal standard. A Hypersil BDS C18 column provided chromatographic separation of analytes followed by detection with mass spectrometry. The method involves a rapid solid-phase extraction from plasma, simple isocratic chromatography conditions and mass spectrometric detection that enables detection at sub-nanogram levels. The proposed method has been validated for a linear range of 0.1-10.0 ng/mL with correlation coefficient >or=0.9990. The intrarun and interrun precision and accuracy were within 10.0%. The overall recovery for amlodipine was 63.67%. Total run time was 3.2 min only.

norvasc 5mg cost 2017-06-20

The results showed that basal P-gp ATPase activity was increased by CJY with half-maximal activity concentration (Km) of 2.9±0.3 μM and the maximal ATPase activity velocity (Vmax) of 265±21 nM · min-1 · mg-1. Kinetic studies on ATPase activity showed the effects of Verapamil (Ver) on CJY-stimulated, CJX1 on Ver-stimulated, and CJX1 on CJY-stimulated P-gp ATPase activity were all non-competitive inhibition, indicating that these substrates buy norvasc can simultaneously but independently bind to diverse sites on P-gp. The combined effects of CJY with Ver, and CJY with CJX1 show that mixtures of both drugs at these fixed-ratios displayed synergistic interactions.

norvasc brand name 2017-09-14

Primary end points were reached in 42 percent of the placebo group and 39 percent of the amlodipine group, representing a 9 percent reduction in the combined risk of fatal and nonfatal events with amlodipine buy norvasc (95 percent confidence interval, 24 percent reduction to 10 percent increase; P=0.31). A total of 38 percent of the patients in the placebo group died, as compared with 33 percent of those in the amlodipine group, representing a 16 percent reduction in the risk of death with amlodipine (95 percent confidence interval, 31 percent reduction to 2 percent increase; P=0.07). Among patients with ischemic heart disease, there was no difference between the amlodipine and placebo groups in the occurrence of either end point. In contrast, among patients with nonischemic cardiomyopathy, amlodipine reduced the combined risk of fatal and nonfatal events by 31 percent (P=0.04) and decreased the risk of death by 46 percent (P<0.001).

norvasc tablet turca 2015-06-08

The BIA has been developed from the perspective of the buy norvasc NHS for a period of 3 years (years 2010-2012).

norvasc generic picture 2017-12-10

Sixty-one cats completed the study. The responder rate was 63% in amlodipine group and 18% in placebo group. Cats receiving amlodipine were 7.9 (95% CI 2.6-24.1) times more likely to be classified as responders when compared to those receiving placebo (P < .001). From a mean (±SD) baseline value buy norvasc of 181 (±12) mmHg, SBP decreased to 154 (±17) mmHg with amlodipine and to 170 (±21) mmHg with placebo (P < .001). The voluntary acceptance rate of amlodipine formulation was 73%.

norvasc with alcohol 2017-09-14

Treatment of hypertension increasingly requires association of drugs. Among them, the association of calcium antagonists with angiotensin converting buy norvasc enzyme inhibitors is a new tempting approach since the two pharmaceutical classes have synergistic effects on blood pressure lowering and target organ protection whereas their effect is antagonistic for adverse events. Numerous large randomized clinical trials have validated this treatment strategy, and new fixed association are being developed. They apply to hypertensive patients, but also to coronary artery disease patients and more generally speaking to high cardiovascular risk subjects.

norvasc 5mg tablet 2017-11-28

1. The safety and efficacy of amlodipine vs enalapril as monotherapy was evaluated in patients with moderate/severe hypertension (supine DBP 105-125 mm Hg, SBP 140-220 mm Hg). 2. After 2 weeks placebo treatment 31 patients were randomised by the technique of minimisation in an Urispas Online observer-blind study to receive once daily treatment with either amlodipine (15 patients) 5-10 mg, or enalapril (16 patients) 5-20 mg for 8 weeks. The study design concluded with 2 weeks placebo treatment. In addition to clinic measurements, home blood pressure monitoring (Copal UA-251) was performed during the study. 3. Clinic supine systolic blood pressure was reduced from 177 to 152 mm Hg (amlodipine) and 183 to 169 mm Hg (enalapril) (95% CI for the intergroup difference -22.1, 0.3, P = 0.06) after 8 weeks treatment. 4. Clinic supine diastolic blood pressure was reduced from 110 to 93 mm Hg (amlodipine) and 109-102 mm Hg (enalapril) (95% CI for the intergroup difference -17.7, -2.7, P < 0.01) after 8 weeks treatment. 5. Home blood pressure recordings confirmed these reductions in blood pressure. Although the reduction in blood pressure was greater for the amlodipine treated group, the differences between treatments were not statistically significant. 6. Both drugs were reasonably well tolerated. The adverse events occurring most frequently in the amlodipine group were headache (5), peripheral oedema (3), upper respiratory infection (3) and anxiety (2). The adverse events occurring most frequently in the enalapril treated patients were headache (6), dizziness (3) and upper respiratory infection (2).

norvasc mg 2015-12-11

The acute hepatitis observed in this elderly patient was probably Naprosyn P Tablet associated with the administration of levofloxacin.

norvasc reviews hypertension 2017-11-03

Changes Compare Celebrex Prices in QoL were assessed by using the Short Form 12 (SF-12) questionnaire completed by 5434 patients (65.9%) at baseline and 4924 patients (59.8%) at the follow-up visit.

norvasc dosage range 2017-11-27

The peroxidation step in lipid transformation is considered to be essential in the pathogenesis of atherosclerosis. Calcium antagonists (CA) appear to have antioxidant effects in addition to their potent vasorelaxant properties. In the present study, we compared the antioxidative efficacy of CA (amlodipine, lacidipine, nifedipine, isradipine, diltiazem, and semotiadil) in the copper-catalysed oxidation of low-density lipoprotein (LDL) with that of glycated(g)/glycoxidated(go) LDL. This issue is of great importance when considering the potential therapeutic use of antioxidant drugs in diabetes-associated vasculopathy. Oxidation of native LDL was inhibited most efficiently (>90%) by lacidipine and semotiadil in the concentration range 10(-4)-10(-3) M. We found, however, a dramatic decrease in antioxidant activity towards g/goLDL as compared to native LDL in all the CA tested. Only lacidipine significantly inhibited copper-mediated oxidation of g/goLDL in the whole concentration range tested (10(-5) M-10(-3) M). This probably resulted from the increased auto-oxidative potential introduced by early and advanced glycation end products (AGE) into the g/goLDL. We noted that coincubation of LDL with 10(-3) M CA and 0.5 M glucose under oxidative/non-oxidative conditions partially or fully restored the antioxidant capacity of the different CA to inhibit the Zithromax Drug Class subsequent copper-catalysed oxidation of the modified LDL. This is a clear indication that CA inhibit glycative or glycoxidative LDL changes during the preceding long-term glycation period. The notion that both oxidative changes and long-term glycation effects were reduced by CA was corroborated by fluorescence analysis, AGE-ELISA, quantitation of lipid peroxidation, and thiobarbituric acid reactive substance (TBARS) measurement of long-term g/goLDL. The strongest antioxidative effects during long-term glycation of LDL were seen with isradipine, lacidipine, nifedipine, and semotiadil. Diltiazem was the only CA that could not prevent TBARS formation in LDL during the long-term glycation period. In contrast, Amadori product formation, as measured by the generation of fructosamines, was not significantly reduced by any CA tested. Thus CA, like other antioxidants, significantly retard AGE formation, while initial glycation reactions, such as Amadori product formation, are only weakly inhibited.

norvasc tab 5mg 2015-09-06

Pharmacokinetic and pharmacodynamic data were compared between elderly and young patients with hypertension who received single intravenous doses of amlodipine, a dihydropyridine calcium antagonist, followed by oral administration of amlodipine up to 10 mg once daily for Ilosone 500 Mg 12 weeks. After intravenous administration, elderly patients had prolonged elimination half-life values (58 +/- 11 vs 42 +/- 8 hr; p < 0.05) caused by decreased clearance (19 +/- 5 vs 7 liters/hr; p < 0.05). Systolic and diastolic blood pressures were significantly decreased from baseline throughout the 3-month treatment period in both groups. After long-term oral administration, elderly and young patients had comparable decreases in mean blood pressure at a given drug plasma concentration. The antihypertensive effect of amlodipine is well correlated with plasma concentration and, at a given concentration, is similar in both elderly and young patients.

norvasc drug card 2017-06-03

This was a 3 month, randomized Desyrel Reviews , blinded-endpoint study in essential hypertensive patients.

norvasc reviews patients 2015-04-15

The present study examined the effect of long-term treatment with amlodipine and MCI-154 (a Ca2+ sensitizer) on progressive cardiac dysfunction and microvasculature in the dilated cardiomyopathic (DCM) hamster heart. After treatment of DCM hamsters (Bio 53.58) with amlodipine or MCI-154 for 15 wk from the age Aciphex 20 Mg of 5 wk, amlodipine and MCI-154 were found to cause an increase in left ventricular percent fractional shortening and decreases in left ventricular diastolic dimension and isovolumic relaxation time in echocardiograms (P < 0.01). A hemodynamic study showed that the diastolic time constant decreased in the amlodipine-treatment group (P < 0.05). In a morphometric study employing a double-staining method that discriminated arteriolar and venular capillaries, amlodipine and MCI-154 caused increases in total capillary density (P < 0.05) and the proportion of venular capillaries (P < 0.05). Moreover, Northern blot analysis showed that the expression of mRNA for vascular endothelial growth factor was significantly increased by amlodipine and MCI-154. They preserve coronary microvasculature in the DCM hamster and might induce angiogenesis of small vessels, thereby contributing to preservation of cardiac systolic and diastolic function.

generic norvasc 10mg 2017-11-30

The aims of the present study were to compare the effects of cilnidipine [L-type/N-type calcium channel blocker (CCB)] and amlodipine (L-type CCB) alone or in combination with the angiotensin II receptor blocker (ARB), valsartan, on blood pressure (BP), kidney function in Dahl salt-sensitive (DS) rats. DS rats fed a high-salt diet were divided into six groups; control (n = 13), two CCB (cilnidipine or amlodipine) groups at 1 mg/kg/day (n = 10), ARB (valsartan) at 10 mg/kg/day (n = 12), cilnidipine + valsartan (CV, n = 12), and amlodipine + valsartan (AV, n = 12). BPs were lower in the combination therapy groups than in those given either drug alone, but only CV inhibited the increase in urinary albumin excretion (UAE) and lowered the glomerular sclerosis score. In addition, AV elevated plasma renin activity and the angiotensin II concentration, and thus failed to inhibit increases in UAE and to lower glomerular sclerosis score. In conclusion, combination therapy with CCB and ARB decreases BP more effectively than either drug alone. When used in combination with valsartan, cilnidipine is more effective than amlodipine for preventing kidney injury.

norvasc dosage 2015-01-06

The combination of benazepril plus amlodipine was shown to be more effective than benazepril plus hydrochlorothiazide in reducing cardiovascular events in the Avoiding Cardiovascular Events through Combination Therapy in Patients Living with Systolic Hypertension (ACCOMPLISH) trial. There was a small difference in clinic systolic blood pressure between the treatment arms favoring benazepril plus amlodipine. Ambulatory blood pressure monitoring provides a more rigorous estimate of blood pressure effects. A subset of 573 subjects underwent ambulatory blood pressure monitoring during year 2. Readings were obtained every 20 minutes during a 24-hour period. Between-treatment differences (benazepril plus amlodipine versus benazepril plus hydrochlorothiazide) in mean values were analyzed using ANOVA. Treatment comparisons with respect to categorical variables were made using Pearson's χ². At year 2, the treatment groups did not differ significantly in 24-hour mean daytime or nighttime blood pressures (values of 123.9, 125.9, and 118.1 mm Hg for benazepril plus amlodipine group versus 122.3, 124.1, and 116.9 for the benazepril plus hydrochlorothiazide group), with mean between-group differences of 1.6, 1.8, and 1.2 mm Hg, respectively. Blood pressure control rates (24-hour mean systolic blood pressure <130 mm Hg on ambulatory blood pressure monitoring) were greater than 80% in both groups. Nighttime systolic blood pressure provided additional risk prediction after adjusting for the effects of drugs. The 24-hour blood pressure control was similar in both treatment arms, supporting the interpretation that the difference in cardiovascular outcomes favoring a renin angiotensin system blocker combined with amlodipine rather than hydrochlorothiazide shown in the ACCOMPLISH trial was not caused by differences in blood pressure, but instead intrinsic properties (metabolic or hemodynamic) of the combination therapies.

norvasc starting dose 2015-12-04

We studied the antioxidant activities of calcium antagonists against autoxidation in rat brain homogenates. The homogenates were incubated for 30 min at 37 degrees C with or without a calcium antagonist and subsequently assayed for lipid peroxide content. Percent inhibition of the lipid peroxidation was used as an index of the antioxidant effect. Dihydropyridine calcium antagonists exhibited concentration-dependent (3-300 micromol/l) inhibitory effects against lipid peroxidation. The relative order of antioxidant potency and associated IC50 values (micromol/l) of the calcium antagonists for inhibition of the lipid peroxidation were as follows: nifedipine (51.5)>barnidipine (58.6)>benidipine (71.2)>nicardipine (129.3)>amlodipine (135.5)>nilvadipine (167.3)>nitrendipine (252.1)> diltiazem (>300)=verapamil (>300). These results suggest that some dihydropyridine calcium antagonists show antioxidant properties. The antioxidant effects of the calcium antagonists may contribute to their pharmacological actions.

norvasc tablet picture 2017-02-11

Forty-two isolates of A. baumannii were collected. Multilocus sequence typing (MLST) assessed the genetic relationship of the isolates. The resistance phenotypes were determined using disc diffusion. The minimum inhibitory concentrations (MICs) of the drugs were determined by broth microdilution. The combined effects of the drugs were determined by a checkerboard procedure. Metallo-β-lactamase (MBL) was determined using the MBL Etest.

comparative dose norvasc 2015-12-28

The assumption of strict superiority was estimated using the mean change in sitting diastolic blood pressure (DBP) at 8 weeks. Safety was monitored through physical examinations, vital signs, laboratory test results, ECG, and adverse events.

norvasc generic price 2017-04-21

The urinary albumin-to-creatinine ratio decreased by 46% in the indapamide SR group and 47% in the enalapril group. Noninferiority of indapamide SR over enalapril was demonstrated (P = .0236; 35% limit of noninferiority) with a ratio of 0.95 (95% CI: 0.68, 1.34). Mean arterial pressure decreased by 18 mm Hg and 15 mm Hg in the indapamide SR and the enalapril groups, respectively (P = .1136). The effects of both treatments seen in these elderly patients were similar to those observed in the main population, although the extent of the reduction in microalbuminuria was slightly higher. Both treatments were well tolerated, and no difference between groups was observed regarding glucose or lipid profiles.

norvasc recommended dosage 2015-09-05

In a prospective, randomized, open-label trial, hypertensive outpatients (≥65 years) who did not achieve their target BP with ARB monotherapy switched to losartan 50 mg/hydrochlorothiazide 12.5 mg (ARB + D) or ARB plus amlodipine 5 mg (ARB + C) for 12 months. Clinic BP and heart rate (HR), measured every 3 months, visit-to-visit variability and seasonal variation were evaluated.

norvasc missed dose 2016-09-06

Amlodipine decreased oxidative stress in the heart and blood and improved the lipid profile in cholesterolfed rabbits. Therefore, it may be considered a useful tool for the reduction of oxidative stress and improvement of lipid profiles in diseases related to atherosclerosis.

norvasc drug information 2017-04-08

Current Controlled Trials ISRCTN51383267.