We randomly assigned 1715 hypertensive patients with nephropathy due to type 2 diabetes to treatment with irbesartan (300 mg daily), amlodipine (10 mg daily), or placebo. The target blood pressure was 135/85 mm Hg or less in all groups. We compared the groups with regard to the time to the primary composite end point of a doubling of the base-line serum creatinine concentration, the development of end-stage renal disease, or death from any cause. We also compared them with regard to the time to a secondary, cardiovascular composite end point.
Regression of LV mass was the larger in patients with the greater decrease in PAC associated with antihypertensive medication regardless of CCB or ARB. Changes in PAC and SBP may be key determinants of regression of LV mass in hypertensive patients regardless of the medication selected.
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These findings suggest that TGF-β1-CTGF axis is activated in dihydropyridine calcium channel blockers-induced gingival overgrowth and exerts a different control on the activation of fibroblasts with a synthetic phenotype. These results also have implications for better understanding mechanisms of fibrosis and the future use of this pathogenic pathway as a therapeutic target in order to limit gingival fibrosis.
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Matrix metalloproteinase-1 (MMP-1) may play an important role in the pathogenesis of atherosclerosis and atherosclerotic plaque rupture. We investigated the effect of the calcium channel blockers amlodipine and nifedipine on the expression of MMP-1 and tissue inhibitor of metalloproteinase-1 (TIMP-1) in endothelial cells (ECs). MMP-1 and TIMP-1 levels in conditioned media of human vascular ECs were measured by enzyme-linked immunosorbent assay. Collagenolytic activity was determined by fluorescence-labeled collagen digestion. The addition of interleukin-1beta (IL-1beta) increased MMP-1 levels in the culture media of ECs. Amlodipine, but not nifedipine, significantly decreased MMP-1 levels in IL-1beta-stimulated ECs. TIMP-1 levels also were significantly increased by IL-1beta, and its expression was slightly decreased by amlodipine, not by nifedipine. Amlodipine significantly inhibited collagenolytic activity in the culture media of IL-1beta-stimulated ECs, whereas nifedipine showed no significant effect on the activity. Our findings revealed that amlodipine, but not nifedipine, inhibits IL-1beta-induced MMP-1 expression in human ECs.
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In the 'Anglo-Scandinavian cardiac outcomes trial-blood pressure lowering arm' (ASCOT-BPLA), a regimen ofamlodipine and perindopril was compared with a classic regimen of atenolol and bendroflumethiazide in over 19,000 hypertensive subjects. Most likely related to a lower systolic blood pressure, a better metabolic profile and inferiority of the comparator atenolol, the trial showed better outcomes for total and cardiovascular mortality, fatal and nonfatal stroke and cardiovascular events and procedures for the combination of newer agents. Additionally, the newer combination was associated with a 30% reduction in new-onset diabetes mellitus. It is expected that these newer drugs will quickly replace the beta-blockers as the medication for patients with high blood pressure.
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A new medium (pH 5.6 reached by addition of 0.1 mol/l acetate buffer, 37 degrees C, 60 min) was established for detecting anti-free radical compounds in the 1,1-diphenyl-2-picrylhydrazyl (DPPH) assay. DPPH bleaching activities of typical antioxidants appeared generally weaker at pH 8.0 (the measured ethanol solution pH by the classical DPPH assay method) than at pH 5.6. Nilvadipine (CAS 75530-68-6), a lipophilic calcium antagonist, enhanced the bleaching much more at pH 5.6 than at pH 8.0. Nifedipine (CAS 21829-25-4) and amiodipine (amiodipine besilate, CAS 88150-42-9) showed some effect, but the other five calcium antagonists failed to bleach DPPH at any pH tested (pH 4.4-8.0). Probucol and beta-carotene (standard antioxidant) showed nearly the same bleaching activity as nilvadipine. Captopril, glutathione and bilirubin were weaker anti-free radical compounds at pH 5.6. No intermediating participation of superoxide radicals and hydroxyl radicals were observed in the DPPH assay, both at pH 8.0 and 5.6. Thus, nilvadipine was shown to be an efficient free-radical scavenger only at around pH 5.6, a weak acidic condition which may occur as a result of inflammation and/or ischemia-reperfusion.
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The purpose of this review is to discuss the current pharmacological options of treatment in calcinosis cutis related to rheumatic diseases.
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A cross-sectional pilot study included 157 dentate patients aged 60 years or more, taking Amlodipine for at least 3 months. Data were collected from past medical records and oral examination. Clinical assessment of GO was correlated with patient's age, gender, drug dosage (2.5, 5 or 10 mg/day), duration of drug therapy (3-4, 4-6, 6-12, 12-24 and >24 months) and also with subjects' plaque index and gingival index scores.
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After 16 weeks 43, 23.5, 23.5 and 8.7% of patients received 150/5, 150/10, 300/5 and 300/10 mg combinations, respectively. At final visit 93.3% of patients had AP <140/90 mm Hg. Mean AP lowering in the total group was -21.7 ± 9.1/-10.9 ± 10.8mm Hg (<0.0001). There were 2 cases of ankle edema (5.7%) but no withdrawals due to unfavorable events. There were no differences between 4 dosing regimens in laboratory and clinical parameters of safety and tolerability.
In the GENRES study, 208 Finnish men aged 35-60 years with moderate hypertension used amlodipine 5 mg, bisoprolol 5 mg, hydrochlorothiazide 25 mg and losartan 50 mg daily, each for 4 weeks as a monotherapy in a double-blind, randomized, placebo-controlled crossover study; that is, each subject received each type of monotherapy in a random order. The treatment periods were preceded and separated by 4-week placebo periods. Ambulatory 24-h and office blood pressure measurements were carried out after all study periods. Data from several biochemical tests were correlated to antihypertensive drug responses.
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Amlodipine at a dose of 2.5 mg per day showed efficacy and good tolerability in elderly hypertensives.
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Diabetic nephropathy is associated with increased albuminuria and accumulation of extracellular matrix proteins within the kidney. Clinical studies have shown some beneficial effects of calcium channel blockers (CCB) on diabetic nephropathy, even though they are generally considered to be less renoprotective than agents that interrupt the renin angiotensin system. However, effects of CCBs on renal injury, and in particular, expression of extracellular matrix proteins in a model of normotensive diabetic nephropathy, are poorly characterized.
We investigated the pleiotropic effects of a calcium antagonist (amlodipine) on early atherosclerosis development in the presence and absence of an HMG-CoA-reductase inhibitor (atorvastatin) in apolipoprotein E*3-Leiden/human C-reactive protein (E3L/CRP) transgenic mice. Male E3L/CRP transgenic mice were fed a cholesterol-containing diet either with or without amlodipine and/or atorvastatin. After 31 weeks, atherosclerosis in the aortic root area was quantified. Treatment with amlodipine did not significantly lower blood pressure, but resulted in a 43% reduction (P < 0.03) of lesion area as compared with the untreated group. Treatment with atorvastatin resulted in an 80% reduction of lesion area as compared with the untreated group (P < 0.001). Combined treatment with amlodipine and atorvastatin decreased the lesion area by 93%, significantly more than either treatment alone (P < 0.008). Plasma C-reactive protein levels were mildly elevated, on average 10 +/- 6 mg/L, and did not differ between groups, neither on baseline nor during treatment. Treatment with amlodipine, independently of blood pressure lowering, reduced atherosclerosis development in E3L/CRP mice. Atorvastatin had a strong anti-atherosclerotic effect, whereas co-treatment with amlodipine enhanced this effect significantly. Plasma C-reactive protein levels were not affected by any of the three treatments.
Thiazide-type diuretics are associated with an increased incidence of diabetes compared with other antihypertensive medications. In this study, we determined the long-term cardiovascular disease (CVD) consequences of incident diuretic-associated diabetes compared with the effects of incident diabetes associated with calcium channel blocker and angiotensin-converting enzyme inhibitor use.
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Endothelial function in elderly hypertensive patients with arteriosclerosis obliterans has not been evaluated. We examined whether antihypertensive drugs improve vasodilatory response to reactive hyperemia of the limbs in elderly hypertensive patients (83 +/- 8 [SD] years) without (n=46, 0.9 < or = ankle-brachial pressure index < or = 1.4) and with (n=24) arteriosclerosis obliterans (ankle-brachial pressure index < 0.2). Patients were randomized for treatment with monotherapy of either temocapril (14 with and 26 without arteriosclerosis obliterans) or amlodipine (10 with and 20 without arteriosclerosis obliterans) for 6 months. Blood flows of the forearms and legs were measured by strain-gauge plethysmography. The vasodilatory response to the release of compression of the forearms and thighs at 200 mmHg or 20 mmHg more than systolic blood pressure for 5 min and to sublingual administration of nitroglycerin (0.3 mg) was assessed. The maximum reactive hyperemic flow in 35 legs with arteriosclerosis obliterans was significantly (p < 0.001) decreased compared to the value in legs in the control hypertensive subjects. Moreover, maximum reactive hyperemic flow in the forearms of patients with arteriosclerosis obliterans was significantly (p = 0.002) decreased compared to that in the control subjects. Blood pressure was similarly decreased by treatment with temocapril or amlodipine. Response to nitroglycerin (0.3 mg) was not changed by either drug. Treatment with temocapril significantly improved maximum reactive hyperemic flow of not only the legs and forearms in control hypertensives but also the legs and forearms in patients with arteriosclerosis obliterans, and attenuated the worsening of activity of daily living in these patients, although treatment with amlodipine did not. These results suggest that the angiotensin-converting enzyme inhibitor temocapril has a beneficial effect on endothelial function in elderly patients with arteriosclerosis obliterans.