Drugs online research references
Clin Sci (Lond). 2001 Mar;100(3):249-57.
Aminoguanidine and ramipril prevent diabetes-induced increases in protein kinase C activity in glomeruli, retina and mesenteric artery.
Osicka TM, Yu Y, Lee V, Panagiotopoulos S, Kemp BE, Jerums G.
Endocrine Unit, Department of Medicine, University of Melbourne, Austin & Repatriation Medical Centre, Heidelberg, Victoria 3084, Australia.
This study investigated the effects of insulin therapy, inhibition of advanced glycation end-product formation with aminoguanidine and angiotensin-converting enzyme inhibition with ramipril on diabetes-related increases in protein kinase C (PKC) activity in the streptozotocin-diabetic rat. PKC activity in the glomeruli, retina and mesenteric artery was increased by 1.5-2-fold after induction of diabetes, and this increase was maintained over 24 weeks. Treatment with insulin at 2 units or 6 units per day attenuated glomerular PKC in proportion to the level of glycohaemoglobin after 4 weeks of diabetes (r=0.68, P<0.0001). The higher dose of insulin prevented the diabetes-related increase in glomerular PKC activity, although blood glucose levels were not normalized. After 8 weeks of diabetes, ramipril completely prevented the diabetes-related increases in PKC activity in the glomeruli, retina and mesenteric artery. By contrast, aminoguanidine treatment resulted in no inhibition of glomerular PKC activity, partial inhibition of retinal PKC activity and complete inhibition of mesenteric artery PKC activity. After 24 weeks of diabetes, both aminoguanidine and ramipril prevented the diabetes-related increases in PKC activity in all three tissues, in parallel with suppression of albuminuria by both agents. Aminoguanidine also prevented diabetes-related increases in retinal permeability at 16 weeks. These results suggest that the organ-protective effects of insulin, aminoguanidine and ramipril in diabetes may be mediated, at least in part, through the differential inhibition of PKC activity in various tissues.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11222110&dopt=Abstract
J AOAC Int. 2001 Jan-Feb;84(1):1-8.
Voltammetric determination of benazepril and ramipril in dosage forms and biological fluids through nitrosation.
Belal F, Al-Zaagi IA, Abounassif MA.
King Saud University, College of Pharmacy, Department of Pharmaceutical Chemistry, Riyadh, Saudi Arabia.
A simple and highly sensitive voltammetric method was developed for the determination of benazepril (I) and ramipril (II). The compounds were treated with nitrous acid, and the cathodic current produced by the resulting nitroso derivatives was measured. The voltammetric behavior was studied by adopting direct current (DCt), differential pulse (DPP), and alternating current (ACt) polarography. Both compounds produced well-defined, diffusion-controlled cathodic waves over the whole pH range in Britton-Robinson buffers (BRb). At pH 3 and 5, the values of diffusion-current constants (Id), were 5.90 +/- 0.40 and 6.66 +/- 0.61 for I and II, respectively. The current concentration plots for I were rectilinear over the range of 1.5-40 and 0.1-30 microg/mL in the DCt and DPP modes, respectively; for II, the range was 2-30 and 0.1-20 microg/mL in the DCt and DPP modes, respectively. The minimum detectabilities (S/N = 2) were 0.015 microg/mL (about 3.25 x 10(-8)M) and 0.012 microg/mL (about 2.88 x 10(-8)M) for I and II, respectively, adopting the DPP mode. Results obtained for the proposed method when applied to the determination of both compounds in dosage forms were in good agreement with those obtained using reference methods. Hydrochlorthiazide, which is frequently co-formulated with these drugs, did not interfere with the assay. The method was also applied to the determination of benazepril in spiked human urine and plasma. The percentage recoveries adopting the DPP mode were 96.2 +/- 1.21 and 95.7 +/- 1.61, respectively.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11234794&dopt=Abstract
J Mol Cell Cardiol. 1999 May;31(5):1033-45.
Differential expression of angiotensin-converting enzyme and chymase in dogs with chronic mitral regurgitation.
Su X, Wei CC, Machida N, Bishop SP, Hankes GH, Dillon RA, Oparil S, Dell Italia LJ.
Department of Medicine, University of Alabama, University Station, Birmingham, Alabama 35294, USA.
The current study tested the hypothesis that angiotensin-converting enzyme (ACE) and chymase expression are subject to different regulatory processes in the heart, as well as the lungs and kidneys and, as a result, have an important effect on the efficacy of ACE inhibitor treatment in modulating tissue angiotensin II (ANG II) levels in heart failure. A total of 18 dogs underwent the induction of mitral regurgitation and were followed for 5 months. Eleven dogs were untreated and seven received the ACE-inhibitor ramipril at a dose of 10 mg PO BID. Seventeen dogs underwent a sham-operation: six of these dogs were treated with ramipril for 3 months (10 mg PO BID) and 11 were untreated and followed for 3 months prior to sacrifice. In mitral regurgitation dogs, ANG II levels were increased >2-fold in left ventricle, lungs, and kidney, but were normalized with ACE inhibitor-treatment only in the left ventricle. In the left ventricle and lungs steady state ACE mRNA levels and ACE activities were increased 2-fold in treated and untreated mitral regurgitation dogs compared to shams (P<0.05, ANOVA). In contrast, chymase mRNA levels were decreased by >50% and chymase activity was increased in left ventricle (LV) of mitral regurgitation dogs (P<0.05). Neither chymase mRNA nor chymase activity could be detected in the kidney; however, kidney ACE mRNA and ACE activity were significantly upregulated in treated and untreated mitral regurgitation dogs (P<0. 05). These results suggest that ACE and chymase expression are regulated differentially in the dog in response to chronic mitral regurgitation and ACE inhibitor treatment. Further, these responses, as well as regulation of ANG II formation, are organ specific. Copyright 1999 Academic Press.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10339353&dopt=Abstract
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