Drugs online research references
Kidney Int. 2001 Jan;59(1):286-94.
Ramipril prolongs life and is cost effective in chronic proteinuric nephropathies.
Ruggenenti P, Pagano E, Tammuzzo L, Benini R, Garattini L, Remuzzi G.
Clinical Research Center for Rare Diseases "Aldo e Cele Dacco" and Center for Health Economics (CESAV), Mario Negri Institute for Pharmacological Research, and Unit of Nephrology, Ospedali Riuniti, Azienda Ospedaliera, Bergamo, Italy.
BACKGROUND: Our objectives were to predict the long-term cost and efficacy of the angiotensin-converting enzyme, ramipril, in patients with nondiabetic chronic nephropathies. METHODS: The time to end-stage renal disease (ESRD) was predicted by two different models based on the rate of glomerular filtration rate decline (DeltaGFR) and incidence of ESRD (events) measured during the Ramipril Efficacy in Nephropathy Trial in 117 and 166 patients, respectively, randomized to comparable blood pressure control with ramipril or conventional therapy. Direct medical costs of conservative and renal replacement therapy were estimated by a payer perspective, and cases more and less favorable to ramipril were computed by a sensitivity analysis. The study took place at the Clinical Research Center for Rare Diseases, "Aldo & Cele Dacco," Bergamo, Italy. Patients included those with chronic, nondiabetic nephropathies and persistent urinary protein excretion rate >/=3 g/24 h. Time to ESRD, survival, and direct costs of conservative and renal replacement therapy are discussed. RESULTS: Both in the DeltaGFR-based or events-based models, ramipril delayed progression to ESRD and prolonged patient survival by 1.5 to 2.2 and 1.2 to 1.4 years, respectively, and saved $16,605 to $23,894 lifetime and $2, 422 to $4203 yearly direct costs per patient. Even in the less favorable hypotheses, ramipril allowed lifetime and yearly cost savings that exceeded 10 to 11 and 20 to 40 times, respectively, the additional costs related to prolonged survival. CONCLUSIONS: In our study population, ramipril prolongs life while saving money because of its beneficial effect on the course of nondiabetic chronic nephropathies.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11135082&dopt=Abstract
Arterioscler Thromb Vasc Biol. 2001 Jan;21(1):61-6.
ACE inhibitor and AT1 antagonist blockade of deformation-induced gene expression in the rabbit jugular vein through B2 receptor activation.
Lauth M, Cattaruzza M, Hecker M.
Department of Cardiovascular Physiology, University of Gottingen, Gottingen, Germany.
Deformation-induced endothelin-1 synthesis in endothelial cells may contribute to the intimal hyperplasia of venous bypass grafts. ACE inhibitors and angiotensin II type 1 (AT(1)) receptor antagonists are capable of reducing vein graft disease. Therefore, the effects of these drugs on endothelial preproendothelin-1 (ppET-1) and smooth muscle endothelin B receptor (ET(B)-R) expression were investigated in isolated perfused segments of the rabbit jugular vein. Pretreatment with ramiprilat (0.3 micromol/L) or irbesartan (0.01 to 1 micromol/L) had no effect on basal ppET-1 or ET(B)-R expression but markedly attenuated the deformation-induced expression of these gene products, and these effects were reversed by the B(2) receptor antagonist icatibant (Hoe 140) and by the NO synthase inhibitor N(G)-nitro-L-arginine. Candesartan (1 micromol/L) mimicked the inhibitory effect of irbesartan. Moreover, reporter gene analysis with a rat ppET-1 promoter-luciferase construct transiently transfected into porcine aortic cultured endothelial cells revealed that the inhibitory effect of both ramiprilat and irbesartan on deformation-induced ppET-1 expression is species independent and mediated at the level of transcription. In addition, RT-PCR analysis detected only AT(1) receptor expression in the endothelium-intact rabbit jugular vein, and neither irbesartan nor ramiprilat affected endothelial NO synthase expression. Thus, ACE inhibitors and AT(1) receptor antagonists are capable of suppressing deformation-induced gene expression in the vessel wall in both an autocrine (ppET-1) and a paracrine (ET(B)-R) manner via a common mechanism of action that constitutes a B(2) receptor-mediated increase in endothelial NO release.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11145934&dopt=Abstract
pharmakologie.uni-kiel.de
1. Recent studies demonstrated that the cardiac calpain system is activated during ischaemic events and is involved in cardiomyocyte injury. The aim of this study was to investigate the contribution of AT(1) and AT(2) receptors in the regulation of calpain-mediated myocardial damage following myocardial infarction (MI). 2. Infarcted animals were treated either with placebo, the ACE inhibitor ramipril (1 mg kg(-1) d(-1)), the AT(1) receptor antagonist valsartan (10 mg kg(-1) d(-1)) or the AT(2) receptor antagonist PD 123319 (30 mg kg(-1) d(-1)). Treatment was started 7 days prior to surgery. On day 1, 3, 7 and 14 after MI, gene expression and protein levels of calpain I, II and calpastatin were determined in left ventricular free wall (LVFW) and interventricular septum (IS). At day 3 and 14 post MI, morphological investigations were performed. 3. Calpain I mRNA expression and protein levels were increased in IS 14 days post MI, whereas mRNA expression and protein levels of calpain II were maximally increased in LVFW 3 days post MI. Ramipril and valsartan decreased mRNA and protein up-regulation of calpain I and II, and reduced infarct size and interstitial fibrosis. PD 123319 did not affect calpain I or II up-regulation in the infarcted myocardium, but decreased interstitial fibrosis. Calpastatin expression and translation were not affected by AT receptor antagonists or ACE inhibitor. 4. Our data demonstrate a distinct, temporary-spatial up-regulation of calpain I and II following MI confer with the hypothesis of calpain I being involved in cardiac remodelling in the late and calpain II contributing to cardiac tissue damage in the early phase of MI. The up-regulation of calpain I and II is partly mediated via the AT(1) receptor and can be reduced by ACE inhibitors and AT(1) receptor antagonists.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11159730&dopt=Abstract
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