Drugs online research references
Eur J Clin Chem Clin Biochem. 1997 Jun;35(6):411-4.
Effects of ramipril on the hormone concentrations in serum of hypertensive patients.
Gronroos PE, Irjala KM, Vesalainen RK, Kantola IM, Leinonen VM, Helenius TI, Forsstrom JJ.
Central Laboratory, Turku University Central Hospital, Finland.
The effects of the angiotensin-converting enzyme inhibitor ramipril on thirteen endocrinological tests were evaluated. These tests comprised serum follitropin, lutropin, prolactin, thyrotropin, free thyroxine, total thyroxine, free triiodothyronine, parathyrin, cortisol, testosterone, sex hormone binding globulin, androstenedione and dehydroepiandrosterone sulphate. Eleven hypertensive outpatients, 9 men and 2 women, treated at the department of internal medicine in Turku University Central Hospital, received 5 mg of ramipril once a day for the study period of four weeks. The above mentioned endocrinological tests were performed before and at the end of the ramipril treatment. Ramipril decreased the value of free thyroxine statistically significantly, p = 0.011, from the mean value of 17.1 pmol/l to the mean value of 16.0 pmol/l when measured with Amerlex-MAB* free thyroxine kit. The mean within-subject difference was -1.10 pmol/l with a 95% confidence interval of -1.87 - -0.33 pmol/l. With the AutoDELFIA free thyroxine kit and with the reference method dialysis+RIA no effect was detected. Other endocrinological tests examined were not affected by ramipril. Since the decreasing effect of ramipril on free thyroxine was detected only with Amerlex-MAB* but neither with AutoDELFIA nor with dialysis+RIA, the effect was concluded to be analytical. The underlying mechanism and the component ultimately interfering with the analysis is unknown.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9228322&dopt=Abstract
Br J Clin Pharmacol. 1998 Feb;45(2):168-9.
Antioxidant power of angiotensin-converting enzyme inhibitors in vitro.
Benzie IF, Tomlinson B.
Department of Nursing & Health Sciences, The Hong Kong Polytechnic University, Hung Hom, Kowloon.
AIMS: There is controversy regarding the potential antioxidant effect of captopril, therefore this study was performed to compare the in vitro antioxidant power of captopril with other angiotensin-converting enzyme (ACE) inhibitors. METHODS: Antioxidant power of captopril, enalapril, fosinopril, perindopril, quinapril and ramipril in aqueous solution was measured using the ferric reducing (antioxidant) power (FRAP) assay; captopril was also measured in ethanolic solution. RESULTS: Only captopril showed significant antioxidant power, demonstrating a stoichiometric factor of 1.0 in this assay. Concentration-related antioxidant power was seen in both aqueous and ethanolic solutions. CONCLUSIONS: Captopril shows antioxidant activity in vitro. This property could be relevant in vivo if captopril is concentrated in membranes, lipoproteins or at other important sites.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9491832&dopt=Abstract
Exp Nephrol. 1999 May-Jun;7(3):229-35.
Ramipril inhibits in vitro human mesangial cell proliferation and platelet-derived growth factor expression.
Grandaliano G, Ranieri E, Monno R, Gesualdo L, Schena F.
Institute of Nephrology, University of Bari, Italy.
Angiotensin-converting enzyme (ACE) inhibitors are antihypertensive drugs that have been shown to reduce proteinuria and to slow down the progression of renal function deterioration in different models of chronic glomerular disease. Major pathogenetic features of progressive glomerular injury leading to glomerulosclerosis are mesangial cell proliferation and platelet-derived growth factor (PDGF) expression. The aim of the present study was to evaluate the effect of ramipril, an ACE inhibitor, on these two potential therapeutic targets. Thus, the effect of ramipril on DNA synthesis, cell proliferation and PDGF A and B chain gene expression in fetal calf serum (FCS)-activated cultured human glomerular mesangial cells was investigated. DNA synthesis was evaluated by tritiated thymidine incorporation, cell proliferation by direct cell counting and cell viability by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT). PDGF A and B chain gene expressions were studied by Northern blot and RT-PCR, respectively. In a dose-dependent manner ramipril inhibited the FCS-induced DNA synthesis and cell proliferation. This effect was not dependent upon a toxic effect as demonstrated by MTT. The antiproliferative effect of ramipril was most likely independent of its ability to inhibit ACE present in the FCS and/or expressed by the cells, since a synthetic peptide that specifically inhibits ACE, at the same molar concentrations, did not inhibit FCS-stimulated DNA synthesis. Moreover, ramipril significantly reduced FCS-induced PDGF A and B chain gene expression. Finally, ramipril completely abolished the PDGF A and B chain gene expression induced by phorbol 12-myristate 13-acetate, a specific protein kinase C activator, suggesting a site of action downstream of this enzyme in the mitogenic signal transduction pathway. Our study would suggest that the modulatory action of ramipril on activated mesangial cell proliferation and PDGF expression is independent of its ability to inhibit ACE and could represent an additional mechanism in the renal protective effects of this drug.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10352363&dopt=Abstract
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