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Adalat (Nifedipine)
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Adalat

Adalat is a high-quality medication which is taken in treatment of hypertension or high blood pressure, angina or chest pain. Adalat acts by relaxing blood vessels (such as veins and arteries), which makes it easier for the heart to pump and reduces its workload.

Other names for this medication:
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Also known as: Nifedipine.

Description

Adalat is a perfect remedy in struggle against hypertension or high blood pressure, angina or chest pain.

Adalat acts by relaxing blood vessels (such as veins and arteries), which makes it easier for the heart to pump and reduces its workload.

Adalat is also known as Nifedipine, Nicardia, Nifedical, Procardia.

Generic name of Adalat is Nifedipine.

Brand names of Adalat are Adalat CC, Procardia, Procardia XL.

Dosage

Adalat should be taken orally with or without food.

It is better to take Adalat at the same time every day. Take on an empty stomach.

Avoid grapefruit juice during treatment with Adalat.

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

Overdose

If you overdose Adalat and you don't feel good you should visit your doctor or health care provider immediately.

Storage

Store at room temperature between 15 and 25 degrees C (59 and 77 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

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

Do not take Adalat if you're pregnant or you plan to have a baby, or you are a nursing mother. Adalat can harm your baby.

Do not use Adalat in combination with salt substitutes or potassium supplements.

If you want to achieve most effective results without any side effects it is better to avoid alcohol.

Avoid grapefruit juice during treatment with Adalat.

Try to be careful using Adalat if you suffer from kidney disease, liver disease, diseases of the heart or blood vessels (sick sinus syndrome), aortic stenosis, heart failure, low blood pressure, or coronary artery disease.

Do not stop taking Adalat suddenly.

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Two simple, sensitive and economical spectrophotometric methods were developed for the determination of nifedipine in pharmaceutical formulations. Method A is based on the reaction of the nitro group of the drug with potassium hydroxide in dimethyl sulphoxide (DMSO) medium to form a coloured product, which absorbs maximally at 430 nm. Method B uses oxidation of the drug with ammonium molybdate and subsequently reduced molybdenum blue is measured at 830 nm. Beer's law is obeyed in the concentration range of 5.0-50.0 and 2.5-45.0 microg ml(-1) with methods A and B, respectively. Both methods have been successfully applied for the assay of the drug in pharmaceutical formulations. No interference was observed from common pharmaceutical adjuvants. The reliability and the performance of the proposed methods are established by point and interval hypothesis tests and through recovery studies.

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We investigated the effects of oral administration of enteric coated aspirin (ASA) on blood pressure and blood pressure variability of hypertension patients before sleep.

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We evaluated insulin sensitivity in two groups of essential hypertensive subjects before and after treatment with either long-acting nifedipine (nifedipine-CR, Adalat CR tablets; Bayer Yakuhin, Osaka, Japan) (n = 10) or metoprolol (n = 9). Insulin sensitivity was evaluated from the steady-state plasma glucose (SSPG) level measured at the steady-state insulin level (20 to 30 microU/mL) using a modification of the SSPG method previously reported.

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Duchenne Muscular Dystrophy (DMD) is a recessive X-linked genetic disease, caused by mutations in the gene encoding dystrophin. DMD is characterized in humans and in mdx mice by a severe and progressive destruction of muscle fibers, inflammation, oxidative/nitrosative stress, and cell death. In mdx muscle fibers, we have shown that basal ATP release is increased and that extracellular ATP stimulation is pro-apoptotic. In normal fibers, depolarization-induced ATP release is blocked by nifedipine, leading us to study the potential therapeutic effect of nifedipine in mdx muscles and its relation with extracellular ATP signaling. Acute exposure to nifedipine (10 µM) decreased [Ca(2+)]r, NF-κB activity and iNOS expression in mdx myotubes. In addition, 6-week-old mdx mice were treated with daily intraperitoneal injections of nifedipine, 1 mg/Kg for 1 week. This treatment lowered the [Ca(2+)]r measured in vivo in the mdx vastus lateralis. We demonstrated that extracellular ATP levels were higher in adult mdx flexor digitorum brevis (FDB) fibers and can be significantly reduced after 1 week of treatment with nifedipine. Interestingly, acute treatment of mdx FDB fibers with apyrase, an enzyme that completely degrades extracellular ATP to AMP, reduced [Ca(2+)]r to a similar extent as was seen in FDB fibers after 1-week of nifedipine treatment. Moreover, we demonstrated that nifedipine treatment reduced mRNA levels of pro-oxidative/nitrosative (iNOS and gp91(phox)/p47(phox) NOX2 subunits) and pro-apoptotic (Bax) genes in mdx diaphragm muscles and lowered serum creatine kinase (CK) levels. In addition, nifedipine treatment increased muscle strength assessed by the inverted grip-hanging test and exercise tolerance measured with forced swimming test in mdx mice. We hypothesize that nifedipine reduces basal ATP release, thereby decreasing purinergic receptor activation, which in turn reduces [Ca(2+)]r in mdx skeletal muscle cells. The results in this work open new perspectives towards possible targets for pharmacological approaches to treat DMD.

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Free oxygen radicals and insufficiency of antioxidants have been implicated in the pathogenesis of hypertension. We determined the effect of edible oils on blood pressure, lipid profiles and redox status in hypertensive patients given antihypertensive therapy (nifedipine-calcium channel blocker).

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A unique transient outward K(+) current (I(to)) has been described to result from the removal of extracellular Ca(2+) from ventricular myocytes of the guinea pig (15). This study addressed the question of whether this current represented K(+)-selective I(to) or the efflux of K(+) via L-type Ca(2+) channels. This outward current was inhibited by Cd(2+), Ni(2+), Co(2+), and La(3+) as well as by nifedipine. All of these compounds were equally effective inhibitors of the L-type Ca(2+) current. The current was not inhibited by 4-aminopyridine. Apparent inhibition of the outward current by extracellular Ca(2+) was shown to result from the displacement of the reversal potential of cation flux through L-type Ca(2+) channels. The current was found not to be K(+) selective but also permeant to Cs(+). The voltage dependence of inactivation of the outward current was identical to that of the L-type Ca(2+) current. It is concluded that extracellular Ca(2+) does not mask an A-type K(+) current in guinea pig ventricular myocytes.

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Evidence exists that calcium antagonists can have effects on neural function. The aim of this work is to analyze the effect of two dihydropyridines, nifedipine and nimodipine, administered for 11 days on the behavior and pain sensitivity of rats. Nociception was tested using the tail electric stimulation test, and behavior parameters using a holeboard. Our results show that chronic administration of nifedipine or nimodipine induces analgesia that can be evaluated by tail withdrawal. However, neither the vocalization nor the vocalization after discharge were modified, so the analgesia may be mediated by spinal mechanisms. Rats treated with nifedipine or nimodipine exhibited a dose-dependent tendency to avoid the center of the field without modification of other parameters, suggesting an increased emotivity in the rats. This conclusion is supported by the fact that anxiogenic or anxiolytic drugs modify the pattern of locomotion without significant changes in other parameters related with the motility. The results from this study suggest the view of a complex mechanism of action underlying nifedipine- and nimodipine-mediated behavioral effects.

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Gingival enlargement is common among patients and can be caused by a variety of etiological factors. The most common reason is poor oral hygiene and high bacterial load that leads to gingival inflammation and enlargement. Other implicated factors include systemic drugs, such as Phenytoin (Dilantin) taken by epileptic patients, Calcium Channel Blockers such as Nifedipine (Procardia) and Verapamil (Calan) for the treatment of hypertension, arrhythmia and angina. Another class of medication associated with gingival enlargement is immunosuppressive agents given to organ-transplant patients to prevent rejection of the new element, such as Cyclosporine. Some enlargements could be associated with other conditions such as puberty, pregnancy or diabetes or be a symptom of a systemic disease (leukemia, Wegener's granulomatosis or sarcoidosis). In rare cases the cause for the enlargement is genetic and termed Hereditary Gingival Fibromatosis (HGF). HGF is a genetic disorder characterized by a progressive enlargement of the gingiva. Histologically, the gingiva is characterized by an accumulation of dense fibrous connective tissue. This is believed to be due to an imbalance between synthesis and degradation of extracellular matrix composed mainly of collagen molecules or due to an alteration in fibroblast proliferation. Different pathogenic mechanisms have been proposed and examined over the years but no precise process has been identified. The main objective of this paper is to discuss this genetic anomaly and support it with clinical cases of a mother and her two children. It will focus on the clinical and histologic characteristics of HGF as well as known biologic and genetic features and treatment modalities.

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Based on the current available evidence, maintenance treatment with a calcium channel blocker after threatened preterm labour does not prevent preterm birth or improve maternal or infant outcomes.

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adalat generic name 2017-12-27

These data suggest that cilnidipine suppressed the development of doxorubicin-induced nephropathy more efficiently than nifedipine does, possibly through inhibiting N-type calcium channel in mice Generic Cymbalta Release .

adalat online 2016-05-04

Platelet aggregation was measured turbidimetrically using an aggregometer. NF-κB and PPAR activation, intracellular Ca2+ mobilization, PKCα activity, surface glycoprotein IIb/IIIa (GPIIb/IIIa) expression and platelet Bystolic Generic Name activation-related signalling pathways were determined in control and nifedipine-treated platelets in the presence or absence of PPAR antagonists or betulinic acid, a NF-κB activator.

adalat cc generic 2017-05-22

The levels of several GABAA receptor subunit mRNAs increase as cerebellar granule neurons migrate to their adult positions and receive excitatory mossy fiber input. Despite the temporal similarity of these increases in transcript expression in vivo, studies in cultured granule neurons demonstrated that the subunit mRNAs are differentially regulated. To address the possibility that neuronal activity regulates transcript expression, GABAA receptor subunit mRNA levels were assessed in cultured granule neurons grown in chemically defined, serum-free medium containing either nondepolarizing (5 mM) or depolarizing (25 mM) KCl concentrations. Whereas the delta subunit mRNA was almost undetectable in cultures maintained in Online Amoxil nondepolarizing medium, an eightfold increase occurred between days 2 and 4 in cultures grown in depolarizing medium. Furthermore, delta subunit transcript expression was reduced by 76 +/- 6% when neurons in depolarizing medium were switched into nondepolarizing medium. The importance of depolarization in the initiation and maintenance of subunit transcript expression in granule neurons was selective for the GABAA receptor delta subunit. These changes in transcript expression involved calcium entry through L-type calcium channels. Nifedipine treatment (1 microM) both reduced intracellular calcium and decreased delta subunit mRNA expression by 79 +/- 4%. Furthermore, inhibition of Ca2+/calmodulin-dependent protein kinases (CaM kinases) by KN-62 (1 microM) also reduced delta subunit transcript expression. These studies demonstrate that KCl-induced depolarization, a condition that mimics the effects of neuronal activity, selectively modulates GABAA receptor delta subunit mRNA expression through a pathway involving calcium entry and activation of a CaM kinase.

adalat watch online 2015-10-30

Age-related vascular diseases are induced by vascular dysfunction, which involves changes in the vasomotor response. The voltage-dependent L-type calcium channel (VDCC) protein is involved in the regulation of vessel function (contraction/relaxation action). In the present study, we evaluated age-related vasomotor function and expression of the signal-related target proteins, including VDCC, using thoracic aorta Antabuse Online Canada from both 8- and 40-week old Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). In contraction experiments using aortic rings, vasomotor responses of both phenylephrine-induced contraction and acetylcholine-induced relaxation were significantly attenuated with age in SHR, whereas WKY did not lose activity with age. Contraction induced by angiotensin II was impaired only for the 40-week old SHR among all the rat groups tested, although enhanced AT1R/reduced AT2R expression with age was observed for both WKY and SHR. In contrast, a vasomotor responsiveness to Bay K 8644 (a VDCC agonist) at the initial contraction phase was significantly attenuated in both 40-week WKY and SHR with significant reduction of VDCC protein expression. The reduced VDCC expression in 40-week old rats significantly lowered the relaxation activity of VDCC blockers, such as verapamil and Trp-His, but did not affect that of nifedipine. Taken together, we provided the first evidence that aging caused a reduction of VDCC expression in rat aorta, irrespective of the rat strain, along with diminishment of the therapeutic potential of VDCC blockers.

adalat generic 2015-11-26

We have previously described that L-type Ca(2 Biaxin Online +) channels' (LTCCs) activation and metabotropic Ca(2+) release from the sarcoplasmic reticulum (SR) regulate RhoA/Rho kinase (ROCK) activity and sustained arterial contraction. We have investigated whether this signaling pathway can be altered in a new experimental model of subarachnoid hemorrhage (SAH). For this purpose, arterial reactivity was evaluated on days 1 to 5 after surgery. A significant increase of basal tone, measured 4 and 60min after normalization, was observed on day 5 after SAH and at 60min on days 2 and 3 after SAH. This phenomenon was suppressed with LTCCs and ROCK inhibitors. We have also studied arterial rings vasoreactivity in response to high K(+) solutions. Interestingly, there were no significant differences in the phasic component of the high K(+)-induced contraction between sham and SAH groups, whereas a significant increase in the sustained contraction was observed on day 5 after SAH. This latter component was sensitive to fasudil, and selectively reduced by low nifedipine concentration, and phospholipase C and SR-ATPase inhibitors. Therefore, our data suggest that the metabotropic function of LTCCs is potentiated in SAH. Our results could provide a new strategy to optimize the pharmacological treatment of this pathological process.

adalat generic name 2015-06-28

All patients received a low Benicar 20mg Generic dose of a calcium channel blocker (nifedipine or amlodipine) to treat Flammer syndrome. As expected, the symptoms of Flammer syndrome were mitigated. To our surprise, the optic nerve compartment syndrome also improved in eight of the 10 eyes (80 %), but remained unchanged in the remainder.

adalat online 2016-10-09

In migrant countries, ethnic origin may represent a complex of cultural, behavioral and possibly genetic differences. These have been shown to influence acute myocardial infarction (AMI) incidence. How ethnic origin may affect survival after AMI is unknown. Data from 5,692 patients included in the Secondary Prevention Reinfarction Israeli Nifedipine Trial (SPRINT) registry were analyzed. Patients were divided into eight different ethnic groups, according to birthplaces from five continents, representing major socio-economic and possibly some Zetia Generic Alternative genetic variation. Mortality was analyzed after adjustment for baseline characteristics known to predict death from coronary artery disease (CAD) using Jews born in Israel as a reference. The odds ratio for in-hospital mortality was higher in women than in men, but unrelated to ethnic origin. The odds ratio for men ranged between 1.08 (95% confidence interval (CI): 0.67-1.73) for Jews born in Eastern Europe and 1.84 (95% CI: 1.07-3.15) for counterparts born in the Middle East. The odds ratio for women ranged between 0.73 in Jews born in Central Europe (95% CI: 0.35-1.50) and 1.45 (95% CI: 0.76-3.15) for Jewish women born in the Balkan countries. Among 4,686 patients surviving the hospital phase, long-term mortality rates (mean follow-up 7.1 +/- 3.5 years) were 43.3% in men and 57.6% in women. Among 3,586 surviving men, the adjusted risk ratios for 10-year mortality varied between 0.92 (95% CI: 0.72-1.18) for men born in Romania and 1.49 (95% CI: 1.07-2.09) for Israeli born Arabs. The variation among men is within the limits of statistical error. However, among 1,100 surviving women, the risk ratio for 10-year mortality differed significantly, from as low as 1.43 (95% CI: 0.84-2.41) in Jewish women born in Central Europe to as high as 2.83 (95% CI: 1.67-4.79) in counterparts born in the Middle East. The latter observations were consistent with the mortality after 3 years. Thus, ethnic origin of Israelis marginally influenced the in-hospital mortality. The long-term prognosis varied significantly among women from different origins but not among men.

adalat cc generic 2015-06-08

Of the 16 children with GRA who developed hypertension, 50% had moderate-severe hypertension (blood pressure [BP] >99th centile for age and sex); 32% had mild hypertension (BP >95th and <99th centile), and 18% had borderline normal BP (BP >90th and <95th centile). Eight of 16 children with hypertension who received directed monotherapy (glucocorticoid suppression or aldosterone receptor/sodium epithelial channel antagonists) maintained BP below the 90th centile. Three additional subjects receiving a combination of directed therapies or a combination of directed therapies and nifedipine were unable to achieve BP control. At GRA diagnosis, 5 of 8 children were normokalemic, and plasma Diamox Generic Equivalent renin activity was suppressed in 5 of 5 subjects.