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Adalat (Nifedipine)

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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.

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Also known as:  Nifedipine.


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.


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.


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


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.


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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P/Q- and T-type Cav are present in human internal mammary arteries and in cerebral penetrating arterioles. P/Q- and T-type calcium channels are involved in the contraction of mammary arteries from hypertensive patients but not from normotensive patients. Furthermore, in cerebral arterioles P/Q-type channels importance was restricted to hypertensive patients might lead to that T- and P/Q-type channels could be a new target in hypertensive patients.

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These results suggest that the celecoxib, DFU, and indomethacin cause relaxation in ciliary muscle precontracted with carbachol. Blockade of calcium channels with nifedipine in ciliary muscle may increase the relaxant effect of celecoxib, DFU, and indomethacin. The topical or systemic use of celecoxib, DFU, and indomethacin with nifedipine can cause blurred near vision due to ciliary muscle relaxation, and in ocular pain conditions caused by ciliary spasm, the pain can be decreased more easily by combined use of these drugs.

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The main purpose of this study was to compare efficacy, tolerability and influence on quality of life (QOL) of nifedipine gastrointestinal therapeutic system (NI) 30-60 mg once a day vs amlodipine (AM) 5-10 mg once a day in elderly patients with mild-moderate hypertension.

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Overall nifedipine GITS was well tolerated by patients with stable symptomatic angina.

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Corpus cavernosum myocytes generate spontaneous tone that contributes to penile detumescence. It is essential to elucidate how tone is generated to fully understand the processes involved in erection. Tissue experiments have shown that blockers of voltage-dependent Ca2+ channels (VDCCs) reduce tone. However, there is also a widespread belief that these channels are poorly expressed in this tissue. Furthermore, it is unclear how VDCC would interact with recently described intracellular Ca2+ waves, which initiate contractions.

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1. Vasoconstrictor effects of melatonin were examined in isolated rat tail arteries mounted either in an isometric myograph or as cannulated pressurized segments. Melatonin failed by itself to mediate observable responses but preactivation of the arteries with vasopressin (AVP) reliably uncovered vasoconstriction responses to melatonin with maxima about 50% of maximum contraction. Further experiments were conducted with AVP preactivation to 5-10% of the maximum contraction. 2. Responses to melatonin consisted of steady contractions with superimposed oscillations which were large and irregular in isometric but small in isobaric preparations. Nifedipine (0.3 microM) reduced the responses and abolished the oscillations. Charybdotoxin (30 nM) increased the magnitude of the oscillations with no change in the maximum response. 3. Forskolin (0.6 microM) pretreatment increased the responses to melatonin compared to control and sodium nitroprusside (1 microM) treated tissues. The AVP concentration required for preactivation was 10 fold higher than control in both the forskolin and nitroprusside treated groups. 4. In isometrically-mounted arteries treated with nifedipine, melatonin receptor agonists had the potency order 2-iodomelatonin > melatonin > S20098 > GR196429, and the MT2-selective antagonist luzindole antagonized the effects of melatonin with a low pK(B) of 6.1+/-0.1. 5. It is concluded that melatonin elicits contraction of the rat tail artery via an mt1 or mt1-like receptor that couples via inhibition of adenylate cyclase and opening of L-type calcium channels. Calcium channels and charybdotoxin-sensitive K channels may be recruited into the responses via myogenic activation rather than being coupled directly to the melatonin receptors. 6. It is proposed that the requirement of preactivation for overt vasoconstrictor responses to melatonin results from the low effector reserve of the melatonin receptors together with the tail artery having threshold inertia. Potentiative interactions between melatonin and other vasoconstrictor stimuli probably also result from the threshold inertia. A simple model is presented and a general framework for consideration of interactions between weak vasoconstrictor agonists and other vasoconstrictor stimuli is discussed.

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Experiments were performed on both INS-1 cell line and rat isolated pancreatic islets. Insulin release was quantified by the homogeneous time-resolved fluorescence method. Variations in [Ca(2+)]i were measured using the ratiometric fluorescent Ca(2+) indicator Fura-2. Ca(2+) channel currents were recorded with the whole-cell patch-clamp technique.

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Ahmadu Bello University Teaching Hospital, Zaria, Nigeria.

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The regulation of nociceptin/orphanin FQ (N/OFQ) gene expression by neuronal activity and by activation of the cyclic AMP signaling pathway in primary neuronal and astroglial cultures is described. Neuronal activity mimicked by veratridine-mediated depolarization profoundly increased N/OFQ gene expression in primary striatal neurons. Calcium entry through L-type, but not N-type, voltage-sensitive calcium channels activated by depolarization appears to be involved, because nitrendipine and nifedipine, but not omega-conotoxin, reduced the induction of N/OFQ expression by veratridine. A selective inhibitor of calcium/calmodulin kinases (KN-62) also antagonized the depolarization-induced increase in N/OFQ mRNA levels, suggesting a role for these enzymes in the activity-dependent induction of N/OFQ gene expression. Constitutively expressed transcription factors may mediate N/OFQ gene expression levels, because veratridine induction of N/OFQ transcription was insensitive to the protein synthesis inhibitor cycloheximide. Regulation of N/OFQ gene expression by depolarization and cyclic AMP is not restricted to striatal neurons, because similar regulation was also observed in neuronal cultures derived from the cerebral cortex. Veratridine did not increase N/OFQ mRNA levels in primary astrocyte cultures; however, elevated intracellular cyclic AMP levels lead to a dramatic, 30-fold induction of N/OFQ mRNA levels in these cells.

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Thirteen psoriatic patients with hypertension during the course of cyclosporin A therapy were treated for 25 months with a calcium channel blocker, sustained-release nifedipine, to study the clinical antihypertensive effects and adverse events during treatment with both drugs. Seven of the 13 patients had exhibited a subclinical hypertensive state before cyclosporin A therapy. Both systolic and diastolic blood pressures of these 13 patients were decreased significantly after 4 weeks of nifedipine therapy, and blood pressure was maintained within the normal range thereafter for 25 months. The adverse events during combined therapy with cyclosporin A and nifedipine included an increase in blood urea nitrogen levels in 9 of the 13 patients and development of gingival hyperplasia in 2 of the 13 patients. Our findings indicate that sustained-release nifedipine is useful for hypertensive psoriatic patients under long-term treatment with cyclosporin A, but that these patients should be monitored for gingival hyperplasia.

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Increased resistance of airways or blood vessels within the lung is associated with asthma or pulmonary hypertension and results from contraction of smooth muscle cells (SMCs). To study the mechanisms regulating these contractions, we developed a mouse lung slice preparation containing bronchioles and arterioles and used phase-contrast and confocal microscopy to correlate the contractile responses with changes in [Ca(2+)](i) of the SMCs. The airways are the focus of this study. The agonists, 5-hydroxytrypamine (5-HT) and acetylcholine (ACH) induced a concentration-dependent contraction of the airways. High concentrations of KCl induced twitching of the airway SMCs but had little effect on airway size. 5-HT and ACH induced asynchronous oscillations in [Ca(2+)](i) that propagated as Ca(2+) waves within the airway SMCs. The frequency of the Ca(2+) oscillations was dependent on the agonist concentration and correlated with the extent of sustained airway contraction. In the absence of extracellular Ca(2+) or in the presence of Ni(2+), the frequency of the Ca(2+) oscillations declined and the airway relaxed. By contrast, KCl induced low frequency Ca(2+) oscillations that were associated with SMC twitching. Each KCl-induced Ca(2+) oscillation consisted of a large Ca(2+) wave that was preceded by multiple localized Ca(2+) transients. KCl-induced responses were resistant to neurotransmitter blockers but were abolished by Ni(2+) or nifedipine and the absence of extracellular Ca(2+). Caffeine abolished the contractile effects of 5-HT, ACH, and KCl. These results indicate that (a) 5-HT and ACH induce airway SMC contraction by initiating Ca(2+) oscillations, (b) KCl induces Ca(2+) transients and twitching by overloading and releasing Ca(2+) from intracellular stores, (c) a sustained, Ni(2+)-sensitive, influx of Ca(2+) mediates the refilling of stores to maintain Ca(2+) oscillations and, in turn, SMC contraction, and (d) the magnitude of sustained airway SMC contraction is regulated by the frequency of Ca(2+) oscillations.

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Experimental subjects underwent caudally based RPSFs using the modified McFarlane technique. Subjects received either topical anti-ischemic drug therapy (nifedipine; n = 6) or inert carrier ointment (placebo; n = 6). Treatment was initiated immediately following flap closure and continued every 6 hours for 5 days. At the end of the treatment period, the animals were killed and the concentration of ET-1 was determined using enzyme-linked immunosorbent assay. Representative tissues from nifedipine- and placebo-treated skin flaps were also analyzed for ET-1 using immunohistochemical stains.

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adalat oros tablet mga 30mg 2017-04-26

In SSc patients, cyclic intravenous iloprost infusion is able to control vasospastic disease. Our results suggest that it might also act as a disease-modifying agent, as it seems to improve the course of the disease. Further studies principally Lopressor Hct Reviews focused on organ involvement and the natural history of the disease are needed to confirm our results.

adalat gits 30 mg 2016-04-03

Decreasing neuronal Ca(2+) levels potentiated buspirone-induced antinociception; conversely, increasing intracellular Ca(2+) abolished the antinociceptive effects of buspirone. These results suggest that Ca(2+) influx from extracellular fluid and release of Ca Lopid Tabs (2+) from Ca(2+)/caffeine-sensitive microsomal pools may be involved in buspirone-induced antinociception.

adalat xl generic name 2015-07-30

TGF-beta1 is a potent osteoactive factor and exhibits a wide variety of effects on osteoblasts, most of which are mediated through receptor associated Smad proteins. We have recently reported a novel TGF-beta1 intracellular Ca2+ signaling pathway in osteoblasts, and found that this signaling is required for the TGF-beta1 mediated enhancement of osteoblast adhesion to substrate. Given that interaction between the extracellular matrix protein fibronectin and alpha5beta1 integrin on the cell surface is principally responsible for osteoblast substrate adhesion, we examined here whether the TGF-beta1 stimulated Ca2+ signal is involved in this pathway. Our results show that, in primary human osteoblasts, the TGF-beta1 induced intracellular Ca2+ signal is responsible, in part, for the stimulation of expression of alpha5 integrin, but not of beta1 integrin or fibronectin. Increased levels of alpha5 integrin protein and mRNA were seen as early as 12 h after TGF-beta1 treatment, but were inhibited by co-treatment of cells with nifedipine, a selective L-type Ca2+ channel blocker. TGF-beta1 treatment increased both fibronectin and beta1 integrin protein production within 48 h, in a manner unaffected by co-treatment with nifedipine. Immunofluorescence observations revealed that TGF-beta1 treatment resulted in increased alpha5 integrin staining, and more prominent alpha5 integrin clustering, with increased co-localization with the actin cytoskeleton, effects that were blocked by co-treatment with nifedipine. The TGF-beta1 induced intracellular Ca2+ signal in human Nolvadex Online Pharmacy Reviews osteoblasts is thus an important mechanistic step in the regulation of alpha5 integrin expression, later contributing to enhanced cell adhesion.

adalat medicine 2017-01-22

Tension development of vas deferens and seminal vesicle to α1-AR activation was significantly inhibited by tamsulosin, nifedipine, and (S)-(+)-niguldipine. Tamsulosin displayed insurmountable antagonism of contractions induced by norepinephrine in the rat vas deferens and seminal vesicle. Ejaculation latency of male rats was not modified by tamsulosin, nifedipine, or (S)-(+)-niguldipine; however, both the number and weight of the seminal plugs recovered from female rats mated with male Valtrex And Pregnancy Dosage rats treated with tamsulosin were significantly reduced.

adalat oros 30 mg bayer 2015-12-08

Nifedipine, proluton depot and bed rest can be used to inhibit contraction in threatened preterm labor. However, when time-to-event test was used, nifedipine took the shortest time for contraction inhibition with statistical significance Singulair 25 Mg .

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The present results indicate that treatment with PBN and FK 506 gives relatively wide windows of therapeutic opportunity in fetal growth retardation induced by transient intrauterine ischemia Cold Sore Zovirax Pills in rats and suggest the possibility of therapeutic intervention after the start of recirculation.

adalat xl reviews 2015-06-19

The neurosecretory bag cells of sexually mature Aplysia californica release egg-laying hormones as part of the reproductive process after a train of action potentials termed afterdischarge. Whole-cell voltage-clamp experiments were performed in cultured cells from sexually immature A. californica to characterize the inward voltage-gated currents for Na+ and Ca2+. The goal of these experiments was to investigate the regulation of excitability during sexual maturation. Na+ currents in bag cells of immature A. californica were similar in several ways to those of mature animals. The Na+ currents activated at voltages less negative than -30 mV and peaked at 10-20 mV in artificial sea water. The time course and pharmacology of bag cell Na+ currents were similar to those of bag cells from mature A. californica, although the Na+ current density was lower in immature A. californica. Na+ currents were inhibited by tetrodotoxin (50 nmol l-1). The Na+ current was relatively insensitive to depolarized holding potentials (Vh), maintaining approximately 50% of peak current amplitude present at Vh = -70 mV throughout the activation range at Vh = -30 mV. In experiments using a 1 s depolarized Vh prior to a test pulse, the half-inactivation voltage (V1/2) was -27 mV. Recovery of immature Na+ current from steady-state inactivation at Vh = -30 mV had a time constant (tau) of 9.5 ms, significantly slower than in mature animals Rulide Generic Name . Ca2+ currents of immature A. californica activated at approximately -30 mV and peaked at approximately 20 mV with 11 mmol l-1 Ba2+ as the charge carrier. The principle differences from mature Ca2+ currents were the low density of the immature Ca2+ currents and their 'run-down' in whole-cell recordings. The pharmacology and V1/2 of bag cell Ca2+ currents were similar to those of L-type Ca2+ currents in mature cells. The Ca2+ currents were inhibited 61 +/- 10% by nifedipine (10 mumol l-1) and were unaffected by omega-conotoxin GVIA (10 mumol l-1). The Ca2+ currents were relatively insensitive to depolarized Vh, activating maximally at Vh = -90, -70 and -50 mV, and maintaining 50% of this peak current amplitude throughout the activation range at Vh = -30 mV. The V1/2 was -23 mV in experiments in which cells were subjected to a 1 s depolarized Vh prior to a test pulse. Na+ current amplitudes were maintained or increased during 1 min of 4 Hz test pulses in bag cells at Vh = -70 mV and Vh = -30 mV. In contrast, Ca2+ current run-down occurred during 1 min of 4 Hz test pulses in seven of 10 cells at Vh = -70 mV and in 12 of 12 cells at Vh = -30 mV. The observed scarcity of Na+ and Ca2+ currents in immature bag cells as well as the specific characteristics of immature bag cell Ca2+ currents make repetitive action potential firing and hormone release less likely than in mature bag cells.

adalat 50 mg 2017-10-18

  Manometric studies on Levaquin 500 Mg Bid the human lower esophageal sphincter (LES) have shown radial asymmetry of the high-pressure zone (HPZ). The aim of this study was to compare the functional properties of human LES clasp and sling muscles, and to look at their relationship with the expression of muscarinic receptors and intracellular Ca(2+) concentration.

adalat liquid filled capsules 2016-06-15

A primigravid woman with a 6-year history of chronic hypertension was evaluated for the sudden onset of uncontrolled hypertension, proteinuria, and hypokalemia at 16 weeks' gestation. An abdominal sonogram revealed Ventolin Hfa Dosage Frequency a left flank mass, and magnetic resonance imaging confirmed that the mass was of renal origin. The worsening hypertension was not controlled with labetolol, methyldopa, nifedipine, or hydralazine, and required a nitroglycerine drip. The patient had left nephrectomy and subsequently miscarried at 19 weeks' gestation. Her blood pressure gradually decreased and normalized within 6 months. A pathologic examination of the renal mass confirmed that it was a juxtaglomerular cell tumor.

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Native myocytes were obtained from individually isolated rat renal afferent and efferent arterioles and from rat tail arteries (TA). TA myocytes, which possess both L- and T-type Ca(2+) currents, served as a positive control. Inward Ca(2+) and Ba(2+) currents (I(Ca) and I(Ba)) were measured in Motilium Review 1.5 mmol/L Ca(2+) and 10 mmol/L Ba(2+), respectively, using the whole-cell configuration. By exploiting known differences in activation and inactivation characteristics and differing sensitivities to nifedipine and kurtoxin, the presence of both L- and T-type Ca(2+) channels in TA myocytes was readily demonstrated. Afferent arteriolar myocytes exhibited relatively large I(Ca) densities (-2.0 ± 0.2 pA/pF) in physiological Ca(2+) and the I(Ba) was 3.6-fold greater. These currents were blocked by nifedipine, but not by kurtoxin, and did not exhibit the activation and inactivation characteristics of T-type Ca(2+) channels. Efferent arteriolar myocytes did not exhibit a discernible voltage-activated I(Ca) in physiological Ca(2+).

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74% of patients had no clinical effects, 4% minor effects, 2% moderate When Will Cozaar Go Generic effects, and 20% other. No deaths or major effects were reported.

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Agonists of I1 imidazolin receptors are a new drug groups which was registered for the treatment of hypertension. Their antihypertensive action is comparable with current antihypertensives (hydrochlorothiazide, enalapril, atenolol, nifedipine retard) and causes Sporanox Alcohol a drop of the systolic BP by cca 15-20 mm Hg and a drop of the diastolic BP by 10-15 mm Hg with a probable normalization of the blood pressure in cca 60% patients with mild to moderate hypertension. Agonists of I1 imidazoline receptors are suitable in particular for the treatment of hypertension associated with metabolic syndrome. Their effect in patients with ischaemic heart disease or after a cerebrovascular attack is not known and despite very promising theoretical prerequisites they are not indicated in patients with chronic heart failure.