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Blocker Atenolol (blocker + atenolol)
Selected AbstractsAn economic evaluation of atenolol vs. captopril in patients with Type 2 diabetes (UKPDS 54)DIABETIC MEDICINE, Issue 6 2001A. Gray Abstract Aims To compare the net cost of a tight blood pressure control policy with an angiotensin converting enzyme inhibitor (captopril) or , blocker (atenolol) in patients with Type 2 diabetes. Design A cost-effectiveness analysis based on outcomes and resources used in a randomized controlled trial and assumptions regarding the use of these therapies in a general practice setting. Setting Twenty United Kingdom Prospective Diabetes Study Hospital-based clinics in England, Scotland and Northern Ireland. Subjects Hypertensive patients (n= 758) with Type 2 diabetes (mean age 56 years, mean blood pressure 159/94 mmHg), 400 of whom were allocated to the angiotensin converting enzyme inhibitor captopril and 358 to the , blocker atenolol. Main outcome measures Life expectancy and mean cost per patient. Results There was no statistically significant difference in life expectancy between groups. The cost per patient over the trial period was £6485 in the captopril group, compared with £5550 in the atenolol group, an average cost difference of £935 (95% confidence interval £188, £1682). This 14% reduction arose partly because of lower drug prices, and also because of significantly fewer and shorter hospitalizations in the atenolol group, and despite higher antidiabetic drug costs in the atenolol group. Conclusions Treatment of hypertensive patients with Type 2 diabetes using atenolol or captopril was equally effective. However, total costs were significantly lower in the atenolol group. Diabet. Med. 18, 438,444 (2001) [source] Environmental risk assessment of human pharmaceuticals in the European Union: A case study with the ,-blocker atenololINTEGRATED ENVIRONMENTAL ASSESSMENT AND MANAGEMENT, Issue S1 2010Anette Küster Abstract ,-Adrenergic receptor blockers (,-blockers) are applied to treat high blood pressure, ischemic heart disease, and heart rhythm disturbances. Due to their widespread use and limited human metabolism, ,-blockers are widely detected in sewage effluents and surface waters. ,-Adrenergic receptors have been characterized in fish and other aquatic animals, so it can be expected that physiological processes regulated by these receptors in wild animals may be affected by the presence of ,-blockers. Because ecotoxicological data on ,-blockers are scarce, it was decided to choose the ,-blocker atenolol as a case study pharmaceutical within the project ERAPharm. A starting point for the assessment of potential environmental risks was the European guideline on the environmental risk assessment of medicinal products for human use. In Phase I of the risk assessment, the initial predicted environmental concentration (PEC) of atenolol in surface water (500,ng L,1) exceeded the action limit of 10,ng L,1. Thus, a Phase II risk assessment was conducted showing acceptable risks for surface water, for groundwater, and for aquatic microorganisms. Furthermore, atenolol showed a low potential for bioaccumulation as indicated by its low lipophilicity (log KOW,=,0.16), a low potential for exposure of the terrestrial compartment via sludge (log KOC,=,2.17), and a low affinity for sorption to the sediment. Thus, the risk assessment according to Phase II-Tier A did not reveal any unacceptable risk for atenolol. Beyond the requirements of the guideline, additional data on effects and fate were generated within ERAPharm. A 2-generation reproduction test with the waterflea Daphnia magna resulted in the most sensitive no-observed-effect concentration (NOEC) of 1.8,mg L,1. However, even with this NOEC, a risk quotient of 0.003 was calculated, which is still well below the risk threshold limit of 1. Additional studies confirm the outcome of the environmental risk assessment according to EMEA/CHMP (2006). However, atenolol should not be considered as representative for other ,-blockers, such as metoprolol, oxprenolol, and propranolol, some of which show significantly different physicochemical characteristics and varying toxicological profiles in mammalian studies. Integr Environ Assess Manag 2010;6:514,523. © 2009 SETAC [source] The combination of atenolol and amlodipine is better than their monotherapy for preventing end-organ damage in different types of hypertension in ratsJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 4 2009Ping Han Abstract Combinations therapy is often used in hypertensive patients whether combination therapy is necessary for preventing end-organ damage is not known. The objective of this study was to determine in four different hypertensive animal models the necessity of adding the calcium channel blocker amlodipine to therapy with the ß-blocker atenolol to modulate end-organ damage. Spontaneously hypertensive rats, DOCA-salt hypertensive rats, two-kidney, one-clip renovascular hypertensive rats and Lyon genetically hypertensive rats were used to study this objective. These animal models have different sensitivities to atenolol and amlodipine. The dosages of therapy employed were 10 mg/kg atenolol alone, 1 mg/kg amlodipine, 10 mg atenolol + 1 mg/kg amlodipine and 5 mg/kg atenolol+0.5 mg/kg amlodipine. BP was continuously recorded in all animals. After determination of baroreflex sensitivity, rats were sacrificed for end-organ damage evaluation. The combination of amlodipine and atenolol had a synergistic inhibitory effect on blood pressure and blood pressure variability, and end-organ damage as compared with monotherapy with atenolol or amlodipine in all animal models. Baroreflex sensitivity also improved with the combination therapy more than with monotherapy. In conclusion, atenolol and amlodipine combination exerts a superior effect on blood pressure, blood pressure variability, baroreflex sensitivity and end-organ damage. The superior effect of the combination was observed in all four models of hypertension. [source] Heart rate reduction by inhibition of If or by ,-blockade has different effects on postsystolic wall thickeningBRITISH JOURNAL OF PHARMACOLOGY, Issue 3 2007L Lucats Background and purpose: Postsystolic wall thickening (PSWT) is part of thickening that occurs after end-systole and represents wasted effort as it does not contribute to ejection. The effects of antianginal drugs on PSWT remain to be established. We compared the effects on PSWT of two agents that reduce heart rate, the ,-blocker atenolol and the selective inhibitor of If current, ivabradine. Experimental approach: Six dogs were prepared to measure wall thickening by sonomicrometry in the conscious state, at rest and during exercise, after administration of saline, atenolol (1mg.kg -1) or ivabradine (1mg.kg -1). Key results: Atenolol and ivabradine similarly reduced heart rate vs saline at rest (about 10-20%) and during exercise (about 30%). Atenolol but not ivabradine decreased dP/dtmax. Concomitantly, PSWT increased with atenolol vs saline at rest (0.35±0.07 vs 0.21±0.03mm, respectively) and during exercise (0.30±0.04 vs 0.15±0.04mm, respectively). In contrast, ivabradine did not alter PSWT. Importantly, atenolol but not ivabradine increased the ratio of postsystolic to systolic wall thickening by 80±23%. This enhanced thickening during diastole with atenolol was accompanied by impeded isovolumic relaxation of the left ventricle, as illustrated by the significant correlation between the isovolumic relaxation time constant , and the postsystolic to systolic wall thickening ratio. None of these effects of atenolol were abolished when heart rate was controlled with atrial pacing. Conclusion and implications: For a similar heart rate reduction at rest and during exercise, ivabradine, but not atenolol, did not alter PSWT and preserved the part of thickening contributing to ejection. British Journal of Pharmacology (2007) 150, 335,341. doi:10.1038/sj.bjp.0706996 [source] Transforming growth factor ,1 genotype and change in left ventricular mass during antihypertensive treatment,results from the swedish irbesartan left ventricular hypertrophy investigation versus atenolol (Silvhia)CLINICAL CARDIOLOGY, Issue 3 2004Pär Hallberg M.D. Abstract Background: Angiotensin II, via the angiotensin II type 1 (AT1) receptor, may mediate myocardial fibrosis and myocyte hypertrophy seen in hypertensive left ventricular (LV) hypertrophy through production of transforming growth factor ,1(TGF-,1); AT1-receptor antagonists reverse these changes. The TGF-(,1 G + 915C polymorphism is associated with in-terindividual variation in TGF- ,1 production. No study has yet determined the impact of this polymorphism on the response to antihypertensive treatment. Hypothesis: We aimed to determine whether the TGF- ,1 G + 915C polymorphism was related to change in LV mass during antihypertensive treatment with either an AT1 -receptor antagonists or a beta1 -adrenoceptor blocker. The polymorphism was hypothesized to have an impact mainly on the irbesartan group. Methods: We determined the association between the TGF-,1 genotype and regression of LV mass in 90 patients with essential hypertension and echocardiographically diagnosed LV hypertrophy, randomized in a double-blind study to receive treatment for 48 weeks with either the AT1 -receptor antagonist irbesartan or the beta1 -adrenoceptor blocker atenolol. Results: Irbesartan-treated patients who were carriers of the C-allele, which is associated with low expression of TGF-,1, responded with a markedly greater decrease in LV mass index (LVMI) than subjects with the G/G genotype (adjusted mean change in LVMI ,44.7 g/m2 vs. ,22.2 g/m2, p = 0.007), independent of blood pressure reduction. No association between genotype and change in LVMI was observed in the atenolol group. Conclusions: The TGF- ,1 G + 915C polymorphism is related to the change in LVMI in response to antihypertensive treatment with the AT1 -receptor antagonist irbesartan. [source] Wastewater treatment plants as a pathway for aquatic contamination by pharmaceuticals in the Ebro river basin (Northeast Spain)ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 8 2007Meritxell Gros Abstract The occurrence of 28 pharmaceuticals of major human consumption in Spain, including analgesics and anti-inflam-matories, lipid regulators, psychiatric drugs, antibiotics, antihistamines, and ,-blockers, was assessed along the Ebro river basin, one of the biggest irrigated lands in that country. Target compounds were simultaneously analyzed by off-line solid-phase extraction, followed by liquid chromatography-tandem mass spectrometry. The loads of detected pharmaceuticals and their removal rates were studied in seven wastewater treatment plants (WWTPs) located in the main cities along the basin. Total loads ranged from 2 to 5 and from 0.5 to 1.5 g/d/1,000 inhabitants in influent and effluent wastewaters, respectively. High removal rates (60,90%) were achieved mainly for analgesics and anti-inflammatories. The other groups showed lower rates, ranging from 20 to 60%, and in most cases, the antiepileptic carbamazepine, macrolide antibiotics, and trimethoprim were not eliminated at all. Finally, the contribution of WWTP effluents to the presence of pharmaceuticals in receiving river waters was surveyed. In receiving surface water, the most ubiquitous compounds were the analgesics and anti-inflammatories ibuprofen, diclofenac, and naproxen; the lipid regulators bezafibrate and gemfibrozil; the antibiotics erythromycin, azithromycin, sulfamethoxazole, trimethoprim, and less frequently, ofloxacin; the antiepileptic carbamazepine; the antihistamine ranitidine; and the ,-blockers atenolol and sotalol. Although levels found in WWTP effluents ranged from low ,g/L to high ng/L, pharmaceuticals in river waters occurred at levels at least one order of magnitude lower (low ng/L range) because of dilution effect. From the results obtained, it was proved that WWTP are hot spots of aquatic contamination concerning pharmaceuticals of human consumption. [source] | ||||||||||