Drugs online research references
J Diabet Complications. 1988 Jan-Mar;2(1):8-11.
Glomerular filtration rate in early experimental diabetes.
O'Brien RC, Allen TJ, Cooper ME, Bach L, Jerums G.
Department of Medicine, Austin Hospital, University of Melbourne, Victoria, Australia.
A noninvasive single injection technique for the measurement of glomerular filtration rate (GFR) using technetium99m diethylene triamine pentaacetic acid (DTPA) was developed for use in the rat. GFR measurements obtained by the technique correlated well with those obtained by Cr51 EDTA infusion (R = 0.95, n = 7). The coefficient of variation was 8.4%. GFR was measured over 4 weeks in diabetic and control rats. GFR increased with time in both groups, with no difference between the groups; however, when corrected for body weight, diabetes was associated with an increased GFR (diabetic 13.6 +/- 1.7 vs. control 10.4 +/- 0.1 ml/min/kg p less than 0.001). Insulin treated rats had higher GFRs than untreated diabetics (p less than 0.05), but GFR/kg was reduced to that of nondiabetic controls. High protein intake in diabetic rats caused an increase in GFR after 1 week of diabetes, but this was not sustained by the fourth week. Genetic hypertension and angiotensin converting enzyme (ACE) inhibition with ramipril had no effect on GFR in diabetic rats. We conclude that serial measurement of GFR in the diabetic rat is accurate and reproducible. Genetic hypertension, high protein intake, and ACE inhibition have little effect on GFR in experimental diabetes.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2968359&dopt=Abstract
Hypertension. 1997 Nov;30(5):1105-11.
Role of endothelial kinins in control of coronary nitric oxide production.
Zhang X, Scicli GA, Xu X, Nasjletti A, Hintze TH.
Department of Physiology, New York Medical College, Valhalla 10595, USA.
The purpose of the present study was to determine whether interventions that promote kinin production or decrease kinin inactivation affect nitric oxide production in isolated canine coronary microvessels. Accordingly, bradykinin (10[-8] to 10[-5] mol/L), ramiprilat (10[-10] to 10[-8] mol/L), A23187 (10[-8] to 10[-6] mol/L), kallikrein (1 to 20 U/mL), and kininogen (0.5 to 10 microg/mL) were used to stimulate endothelium-dependent nitric oxide production. Receptor antagonists, serine protease inhibitors, and a kinin antibody were used to inactivate local kallikrein-kinin activity. Nitrite, the metabolite of nitric oxide in aqueous solution, was measured using the Griess reaction. All the agonists significantly increased nitrite release. For instance, the highest dose of bradykinin, ramiprilat, A23187, kallikrein, and kininogen markedly increased nitrite production, from 60+/-10 to 156+/-12, 153+/-11, 161+/-15, 176+/-15, and 168+/-16 pmol/mg (all P<.05), respectively. The increased nitrite production caused by these agents was not only blocked by N omega-nitro-L-arginine methyl ester (L-NAME) and HOE 140 (which blocks B2 kinin receptor) but by the kinin antibody also. For instance, nitrite production elicited by bradykinin, ramiprilat, A23187, and kininogen was reduced to 95+/-8, 87+/-8, 94+/-11, and 85+/-11 pmol/mg (all P<.05), respectively, by the kinin antibody. Carbachol-induced nitrite production (from 66+/-8 to 144+/-13) was blocked by L-NAME but not by HOE 140 or the kinin antibody. These results suggest that either increasing kininogen to promote endogenous kinin formation or inhibiting angiotensin-converting enzyme to decrease kinin breakdown, increases nitric oxide production in isolated coronary microvessels. These data indicate that a microvessel kallikrein-kinin system has an important role in the control of nitric oxide production in coronary microvessels.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9369263&dopt=Abstract
Cytokine. 1995 Aug;7(6):526-33.
Angiotensin-converting-enzyme inhibitors suppress synthesis of tumour necrosis factor and interleukin 1 by human peripheral blood mononuclear cells.
Schindler R, Dinarello CA, Koch KM.
Department of Nephrology, Medical School Hannover, Germany.
Administration of angiotensin-converting-enzyme (ACE) inhibitors reduce vascular proliferation following endothelial injury as well as progression of renal disease in various animal models. These effects might be due to interference with cytokines such as interleukin 1 (IL-1) or tumour necrosis factor alpha (TNF) since they have been implicated in regulating the effects of vascular cell growth factors such as fibroblast- and platelet-derived growth factors. We investigated the in vitro synthesis of IL-1 and TNF from human peripheral blood mononuclear cells (PBMC) in the presence of various ACE-inhibitors. Captopril dose-dependently suppressed the IL-1 beta-induced synthesis of TNF by 74% (P < 0.01) and the IL-1 beta-induced synthesis of IL-1 alpha by 60% (P < 0.01). Cytokine synthesis induced by lipopolysaccharide was less affected. At concentrations suppressing TNF and IL-1, captopril did not reduce the synthesis of complement C3 in the same cells. Enalapril and cilazapril also suppressed cytokine-induced cytokine synthesis. Ramipril, lisinopril, perindopril and spirapril had no significant effect on TNF synthesis suggesting that the effect was not related specifically to the inhibition of ACE. Accumulation of mRNA for IL-1 and TNF were not affected by captopril, suggesting a posttranscriptional effect. We conclude that certain ACE-inhibitors suppress IL-1 and TNF synthesis at a posttranscriptional level and might therefore influence cytokine-mediated cell growth.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8580368&dopt=Abstract
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