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Nifedipine is a classical dihydropyridine calcium channel blocker (CCB) indicated for the management of hypertension, vasospastic angina and chronic stable angina. Prestigious regulatory bodies like USFDA, EMA, CDSCO and TGA have approved long-acting Nifedipine for the management of hypertension and angina. Nifedipine was 1st introduced in United States as Adalat® (Bayer) in 1981 and in India as Nicardia® (J. B. Chemicals & Pharmaceuticals) in 1985. Conventional Nifedipine shows the rapid onset and short duration of action which results in prompt and marked hypotensive effect but exhibits reflex SNS activation leading to flushing, tachycardia, worsening myocardial ischemia, and cerebrovascular ischemia. Nifedipine gastrointestinal therapeutic system (GITS) formulation addresses many of the concerns surrounding the older formulations of Nifedipine. Nifedipine GITS is a gold standard once-daily formulation of Nifedipine which allows relatively constant plasma drug concentrations over 24 hours. Nifedipine GITS provides a controlled release and gradual onset of action of Nifedipine, avoiding the reflex SNS activation resulting in improved tolerability and compliance. Clinical studies suggest that long-acting formulations of Nifedipine have slightly greater antihypertensive actions than Amlodipine. Nifedipine was also found to be more efficient than other CCBs like Amlodipine, Nicardipine, and Isradipine in resistant hypertensive patients. The addition of Nifedipine GITS to the conventional treatment of angina pectoris is safe and reduces the need for coronary angiography and interventions. Several landmark trials have demonstrated that long-acting Nifedipine improves endothelial function and arterial stiffness and reduces albuminuria, LV hypertrophy, atherosclerotic plaques and cardiovascular and cerebrovascular complications. This comprehensive review focuses on the superiority of the Nifedipine GITS formulation over the conventional Nifedipine and elaborates on the role of long-acting Nifedipine as a CCB of choice for the management of hypertension, resistant hypertension, angina pectoris and coronary artery disease. [ABSTRACT FROM AUTHOR]

Aim. To compare effects of enalapril in combination with long-acting nifedipine or moxonidine on blood pressure (BP), myocardial mass and diastolic function of left ventricular, lipid and carbohydrate metabolism, platelet aggregation in patients with arterial hypertension (HT) and metabolic syndrome (MS).Material and methods. 50 patients with HT and MS were examined. 25 patients were treated with enalapril and long-acting nifedipine and 25 patients – with enalapril and moxonidine. 24-hour BP monitoring, echocardiography, anthropometry, lipid and carbohydrate metabolism estimation, platelet aggregation testing were performed before and 6 months after treatment.Results. Both combinations allowed to achieve target BP levels, provided cardioprotective and positive metabolic effects in most patients. The combination of enalapril and long-acting nifedipine had more significant antihypertensive effect and more prominently decreased the platelet aggregation induced by collagen. The combination of enalapril and moxonidine had more significant positive effects on carbohydrate metabolism and ADP-induced platelet aggregation.Conclusion. Enalapril in combination with long-acting nifedipine or moxonidine can be recommended for treatment of patients with HT and MS.

Nifedipine, a dihydropyridine calcium antagonist, improves endothelial function in patients with hypercholesterolaemia by enhancing nitric oxide (NO) activity, and increases endothelial NO bioavailability by antioxidant mechanisms. We administered a long-acting nifedipine formulation (controlled release (CR) nifedipine: 20 mg/day) to hypertensive patients for 6 months. There were no other changes of drug treatment during therapy with CR nifedipine. Clinical and biochemical data obtained before and after CR nifedipine administration were compared. All markers were measured by enzyme-linked immunosorbant assay. The levels of soluble markers (soluble CD40 ligand, soluble P-selectin, and soluble E-selectin), microparticles (MP) (platelet-derived MP, monocyte-derived MP, and endothelial cell-derived MP), and adiponectin differed between the control group and the hypertension group. The levels of these markers were also different in hypertensive patients with and without type 2 diabetes compared with the control group. In the hypertensive patients with type 2 diabetes, all markers except adiponectin decreased significantly after 3 months of CR nifedipine treatment. In contrast, markers were unchanged in the hypertensive patients without type 2 diabetes. Adiponectin was increased after 6 months of CR nifedipine treatment in hypertensive patients with type 2 diabetes. The effects of CR nifedipine on platelet/monocyte activation and adiponectin levels demonstrated in the present study indicate the potential effectiveness of calcium antagonist therapy for hypertensive patients with type 2 diabetes.Journal of Human Hypertension (2007) 21, 38–44. doi:10.1038/sj.jhh.1002100; published online 19 October 2006 [ABSTRACT FROM AUTHOR]

Background: Experimental and clinical evidence suggests that calcium-channel blockers may retard the atherosclerotic process after long-term treatment. Whether these effects exist after intermediate-term treatment in hypertensive patients is mainly unknown. Objective: To determine the 26-week effects of the long-acting calcium-channel blocker nifedipine on intima media thickness (IMT) in newly found hypertensive patients. Design: Open-label study with blinded end-point analysis. Methods: From a population survey, 131 previously untreated mild hypertensives (4× systolic blood pressure between 160 and 220 mmHg and/or diastolic blood pressure between 95 and 115 mmHg) were included. Patients were treated with long-acting nifedipine 30-60 mg targeted to reach a predetermined drop in blood pressure. Prior to and after 26 weeks of treatment, IMT was measured by ultrasonography in the carotid and femoral artery. The combined mean maximal far wall IMT was used as primary endpoint. Change from baseline was evaluated by paired t-test in an intention-to-treat analysis. Results: The mean maximal far wall IMT at baseline was 1.03 ± 0.23 mm, and decreased by 0.078 mm (95% confidence interval, CI 0.044-0.111) after treatment. Regression analysis, including baseline IMT and changes of blood pressure, showed that reduction of IMT was mostly influenced by baseline IMT ( p < 0.001; model R [Formula: See Text] = 0.11). Conclusion: Our observations show that 26 weeks of nifedipine treatment inhibits IMT progression in these newly found hypertensive patients. This effect was mostly seen in arterial walls with highest IMT before treatment, suggesting that patients with highest cardiovascular risk benefit most of antihypertensive treatment. [ABSTRACT FROM AUTHOR]