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There are several concerns with this trial (25): 1) the mean (±SD) of diastolic blood pressure in the nifedipine group was 78 ± 11 mm Hg. In patients with chronic severe AR, this measure is very much lower, which suggests that most patients in the nifedipine group did not have severe AR. Moreover, the LV end-diastolic volume index was 94 ± 27 ml/m2, whereas in the Padua trial it was 126 ± 16 ml/m2 (26), which supports that many patients in the Barcelona trial did not have chronic severe AR; 2) there were 32 patients in the nifedipine arm, 7 (22%) dropped out at 2 ± 7 months, thus, only a small number of patients were randomized. In the Padua trial there were 69 patients in the nifedipine group and 4 were lost to follow-up; and 3) there was no change in blood pressure in the Barcelona trial in which nifedipine 20 mg twice a day was given. In the Padua trial, long-acting nifedipine 20 mg was given twice a day, and at the end of the trial there were significant reductions of LV volumes and ...
In a multicenter double-blind study, 227 patients with suspected acute myocardial infarction (AMI) were randomized within 12 hr from onset of symptoms to treatment with nifedipine (112 patients) or placebo (115 patients). AMI was confirmed in 74 patients on nifedipine and in 83 on placebo. Patients with AMI received nifedipine 5.5 +/- 2.9 hr (mean +/- SD) after onset of symptoms. Infarct size was assessed by the release of creatine kinase isoenzyme MB (CK-MB). Infarct size index (CK-MB geq/m2) was 25 +/- 16 (n = 71) in the nifedipine group and 23 +/- 13 (n = 77) in the placebo group (NS). After the first 10 mg of nifedipine systolic blood pressure fell from 147 +/- 30 to 135 +/- 28 mm Hg (p less than .01) and heart rate rose from 75 +/- 18 to 79 +/- 19 beats/min (p less than .01). No change was observed after the first placebo dose. The treatment was continued for 6 weeks. Over this period there were 10 deaths in each group. Early treatment with nifedipine in patients with AMI does not seem to ...
Dihydropyridines (DHP), which nifedipine is a member of, preferentially block Ca2+ channels of different cell types. Moreover, influx of Ca2+ through L-type Ca2+ channels (LTCCs) activates Ca2+ signaling pathways, which in turn contribute to numerous cellular processes. Although LTCCs are expressed in undifferentiated cells, very little is known about its contributions to the transcriptional regulation of mesodermal and cardiac genes. This study aimed to examine the contribution of LTCCs and the effect of nifedipine on the commitment of pluripotent stem cells toward the cardiac lineage in vitro. The murine embryonic stem (ES, cell line D3) and induced pluripotent stem (iPS, cell clone 09) cells were differentiated into enhanced green fluorescence protein (EGFP) expressing spontaneously beating cardiomyocytes (CMs). Early treatment of differentiating cells with 10 µM nifedipine led to a significant inhibition of the cardiac mesoderm formation and cardiac lineage commitment as revealed by gene regulation
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Pain. Pancreatitis. Abstract. Endoscopic retrograde cholangiopancreatography (ERCP) is complicated by acute pancreatitis in up to. Digestion. 1993;54(2):105-11. Prospective randomized trial of the effect of nifedipine on pancreatic irritation after endoscopic retrograde. The aim of this randomized, placebo-controlled trial was is zoloft a generic xanax determine whether the calcium channel blocker nifedipine prevents post-ERCP pancreatitis.. We excluded other causes of acute pancreatitis by clinical history, serum Keywords: Pancreatitis • Nifedipine • Acetaminophen • Poisoning • Hemofiltration. ...
The present study highlights the following novel findings on the mechanisms responsible for the normalization of endothelial dysfunction by calcium antagonists. (1) The calcium antagonist nifedipine indirectly upregulates SOD activity and expression in ECs through activation of adjacent VSMCs. (2) VEGF released from VSMCs is involved in the mechanism underlying the upregulation of endothelial SOD activity by nifedipine. (3) Nifedipine stimulates the release of VEGF from VSMCs through activation of the bradykinin B2 receptor. (4) Upregulation of endothelial SOD by nifedipine results in the enhancement of NO production from ECs.. Calcium antagonists are widely used in the treatment of hypertension and angina pectoris. Recent evidence suggests that these drugs improve clinical outcome in patients with certain cardiovascular diseases.12,13⇓ It is noteworthy that calcium antagonists have been shown to normalize endothelial dysfunction in many cardiovascular diseases,14 because endothelial ...
It is known that various DHP calcium antagonists enhance the NO release from endothelial cells.14 15 16 17 18 19 Using an NO-sensitive electrode, we previously demonstrated that nifedipine in the micromolar and submicromolar concentration ranges stimulates the NO release from the native endothelium.33 34 These findings were obtained after acute exposure to DHP calcium antagonists. Therefore, we investigated whether (1) a long-term treatment (48 hours, entire passage 2) of porcine endothelial cell cultures with nifedipine resulted in a similarly altered NO release and (2) an increased formation and/or an impaired inactivation of NO might be involved by measuring the ecNOS (NOS isoform III) mRNA and protein expression and the antioxidative potency of nifedipine, respectively.. In contrast to the short-term measurements during long-term treatment, nifedipine was not present in the buffer during the antioxidative and NO experiments.. We could demonstrate that treatment with nifedipine (concentration ...
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In a double-blind, randomized crossover study, the daily administration of 30 to 90 mg of nifedipine lowered blood pressure in a dose-related fashion in 14 patients already taking a beta receptor blocker and diuretic. The duration of the hypotensive response to 20 mg of nifedipine in capsule form, giving as a step-three drug to five of these patients, was six to eight hours. A survey of 122 patients with resistant hypertension treated long-term with nifedipine and a control group of 102 similar patients treated with hydralazine revealed that nifedipine at an average dose of 40 mg daily caused a fall in blood pressure similar to that achieved with hydralazine in a dose of 86 mg daily. The side effect profile of both drugs was also similar. Nifedipine may be a useful alternative to existing step-three antihypertensive drugs.
I read an article online today about nilvadipine blocking the syk enzyme. I found your blog post just now when I was googling for more information on nilvadipine. I am hoping I can find nilvadipine here in Mexico where I live. I went to 3 pharmacies today but so far nobody has it. All I can find is nifedipine, which I think is not the same thing. Ive been taking atacand for years for my high blood pressure but Id sure like to switch to nilvadipine. I also have diabetes. My mother had Alzheimers. She also had high blood pressure. If I find nilvadipine here in Mexico, Ill let you know.. ReplyDelete ...
Quite unexpectedly, it was found that the asymmetrical nonlinear behavior of ΔVm was reversed by application of Ca2+ channel blocker nifedipine. As seen in Figures 2⇑ and 4⇑, nifedipine caused a strong increase in the magnitude of the maximal positive ΔVm, but either no change (wide strands) or a decrease (narrow strands) of the negative ΔVm. In both cases, the ΔVm asymmetry was strongly reduced.. As we argue below, the effect of nifedipine on the ΔV−m in the narrow strands was not direct but was mediated via electrotonic interaction with the area of positive ΔVm. Thus, the key effect of nifedipine was the increase of the ΔV+m. In general, 2 different explanations for this effect are possible. First, nifedipine could directly affect the ΔV+m. Second, similarly to the effect of 4-AP, nifedipine could affect APA, thus changing the optically measured ΔV+m. Although it is known that nifedipine can slightly reduce APA in neonatal rat myocytes,15 this effect does not explain the ...
Taking a shorter acting of antibiotics may be nifedipine dosage hypertension as effective, nifedipine dosage hypertension do a better job at using antibiotic resistance. ANyone had a 7 day regimen for amoxicillin for ear infection. Sadly, I liked antibiotics for my son, without street him a chance to see if he. You subdue taking antibiotics as soon as you would better. Your flush gives you seven to 10 days worth of pills. Nifedipine, Oral Tablet. Nifedipine oral tablet is a prescription drug thats available as the brand-name drugs Adalat CC, Afeditab CR, and Procardia XL. Nifedipine is used to lower blood pressure in people with hypertension.‎About · ‎Interactions · ‎Other warnings · ‎Dosage. Medscape - Indication-specific dosing for Procardia, Procardia XL (nifedipine), frequency-based adverse effects, comprehensive interactions, contraindications, pregnancy & lactation schedules, and cost information.. ...
Nifedipine is completely absorbed after oral administration. Plasma drug concentrations rise at a gradual, controlled rate after a Nifedipine Extended-release Tablet dose and reach a plateau at approximately six hours after the first dose. For subsequent doses, relatively constant plasma concentrations at this plateau are maintained with minimal fluctuations over the 24-hour dosing interval. About a fourfold higher fluctuation index (ratio of peak to trough plasma concentration) was observed with the conventional immediate-release nifedipine capsule at t.i.d. dosing than with once daily Nifedipine Extended-release Tablet. At steady-state the bioavailability of the Nifedipine Extended-release Tablet is 86% relative to immediate-release capsules. Administration of the Nifedipine Extended-release Tablet in the presence of food slightly alters the early rate of drug absorption, but does not influence the extent of drug bioavailability. Markedly reduced GI retention time over prolonged periods (i.e., ...
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We investigated the effect of the calcium channel antagonist nifedipine on the induction of nitric oxide synthase (NOS) by bacterial endotoxin (lipopolysaccharide; LPS) in J774.2 macrophages, in cultured rat aortic smooth muscle cells and in a rat model of endotoxin shock. Stimulation by LPS for 24 hr increased nitrite accumulation in the supernatant of both cell types. NOS induction accounts for this nitrite accumulation, as both NG-methyl-L-arginine and cycloheximide reduced nitrite production in both cell types. Dexamethasone inhibited LPS-stimulated nitrite production in macrophages, but not in rat aortic smooth muscle cells. Nifedipine inhibited the production of nitrite in these LPS-treated cell types, with a more pronounced effect on macrophages. However, nifedipine did not inhibit the production of nitrite in J774.2 cells in which NOS had already been induced by prior exposure to LPS, and any possible further induction was inhibited by cycloheximide. In anesthetized rats subjected to ...
The present study provides 2 major new findings. First, in contrast to its peripheral effects, centrally administered nifedipine decreases RSNA and HR in conscious SHR. Second, these sympathoinhibitory effects of nifedipine are enhanced in SHR on high versus regular sodium intake.. Dihydropyridine-sensitive, low-voltage-activated calcium channels have been demonstrated in rat brain neurons freshly isolated from regions such as the ventromedial hypothalamus.6 The role of the different types of calcium channels in neuronal synaptic transmission has not been clarified. In rat hippocampal cells,7 during neuronal activation postsynaptic or presynaptic Ca2+ entry involves the activation of the P/Q-, L-, or N-type Ca2+ channels but not the T-type Ca2+ channels. Unless dissolved in certain solvents such as dimethylsulfoxide,15 nifedipine blocks only L-type channels and has no effects on T-type channels in neuronal cells.8 15 In the present study nifedipine was dissolved in a vehicle containing no ...
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A form of human hepatic microsomal cytochrome P-450 (P450hA7) with subunit Mr 50,400 has been purified from an epileptic who had been receiving long-term treatment with anticonvulsant drugs. P450hA7 metabolized the immunosuppressant drug cyclosporin A and the dihydropyridine calcium channel antagonist nifedipine, but did not metabolize a similar dihydropyridine drug, nicardipine, nor a series of alkoxyresorufin model substrates. The hepatic microsomal concentration of P450hA7 was higher in five individuals who had been receiving long-term anticonvulsant treatment than in any of 21 individuals who had not been similarly treated. The mean P450hA7 concentration in the treated individuals was 5-fold higher than the mean concentration in the untreated individuals. It is concluded that P450hA7 is a member of the cytochrome P450III family which is induced by anticonvulsant drugs in man. ...
Early treatment with nifedipine in patients with AMI did not appear to reduce infarct size as determined by enzyme level. Although blood pressure reduction was achieved with nifedipine, there was no observed clinical benefit. In a similar fashion, the Trent nifedipine study observed no mortality benefit from nifedipine after myocardial infarction. The investigators concluded that there was no reason to recommend general treatment with calcium antagonists to reduce infarct size.. ...
TY - JOUR. T1 - Comparison of myocardial protection with nifedipine and potassium. AU - Magee, P. G.. AU - Flaherty, J. T.. AU - Bixler, T. J.. AU - Glower, D.. AU - Gardner, T. J.. AU - Bukley, B. H.. AU - Gott, V. L.. PY - 1979/1/1. Y1 - 1979/1/1. N2 - Nifedipine, a slow-channel calcium blocker, is thought to provide useful myocardial protection during prolonged total ischemia and reperfusion. An isolated, isovolumic, feline heart model was used to assess the effectiveness of nifedipine in both cardioplegic (100 μg/10 ml) and noncardioplegic (10 μg/10 ml) doses for providing myocardial preservation during 90 minutes of hyperthermic ischemic arrest and 45 minutes of normothermic reperfusion. Use of nifedipine was compared to hypothermia (27°C) alone and to hypothermia with potassium cardioplegia. Ventricular function was assessed by recovery of isovolumic left ventricular developed pressure and dP/dt. Myocardial carbon dioxide tension (PCO2) and myocardial oxygen tension (PO2) were measured ...
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To compare renal function (51Cr-EDTA clearance) 48 hours post open-heart surgery (coronary bypass or valve surgery) in patients with impaired renal function after randomization to either nifedipine infusion at start of surgery and the following 24 hours or placebo (0.9% saline infusion). Study hypothesis is that nifedipine has a prophylactic effect on decline in renal function ...
INSIGHT and NORDIL add to the acronymic litany of recent trials addressing pharmacotherapy of hypertension-this litany consists of multiple trials with multiple comparisons spawned by multiple drugs from multiple classes with multiple actions. With the addition of the INSIGHT trial and NORDIL study, we have 10 completed long-term trials that compare calcium antagonists with other antihypertensive drugs. Such trials that evaluate morbidity and mortality effects of calcium antagonists have variable findings that are difficult to interpret. • None were large enough to reliably detect moderate differences (10% to 15%) in such clinically important outcomes as MI (1). • BP control with monotherapy was not achieved in as many as one third to one half of trial participants, depending on baseline and target BP levels. • Comparisons among agents were usually complicated by the addition of second and third drugs. • In large trials, such as INSIGHT and the Swedish Trial in Old Patients (STOP-2) (2), ...
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The signaling pathways following histamine H3 receptor activation by (R)alpha-methylhistamine (MHA) have been examined in the isolated guinea pig duodenum, in which selective excitation of cholinergic neurons was induced by electrical field stimulation (EFS). The effect of MHA on electrically evoked contractions was compared with that induced by the alpha-2 adrenoceptor agonist clonidine (CLON). The inhibitory effect of MHA on EFS-induced contractions was significantly reduced by increasing CA++ content in the nutrient fluid from 2.5 to 5 mM and by the Ca++ agonist Bay K 8644 (10(-8) M); conversely, the effect of MHA was significantly enhanced by lowering Ca++ content in the medium (from 2.5 to 1.25 mM) and by the N-type Ca++ channel blocker omega-conotoxin (CTX) (10(-8) M). The L-type Ca++ channel blocker nifedipine (NIF) (10(-7) M) did not modify the effect of MHA, although it significantly reduced both EFS- and exogenous acetylcholine (ACH)-induced contractions. Similar to MHA, the inhibitory ...
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Ask your health care provider any questions you may have about how to use Adalat.. STORAGE. Store Adalat at room temperature, between 59 and 86 degrees F (15 and 30 degrees C). Store away from heat, moisture, and light. Do not store in the bathroom. Keep Adalat out of the reach of children and away from pets.. MORE INFO:. Active Ingredient: Nifedipine.. ...
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