Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/9325
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dc.contributor.authorCao, Zeminen
dc.contributor.authorBurrell, Louise Men
dc.contributor.authorTikkanen, Ilkkaen
dc.contributor.authorBonnet, Fabriceen
dc.contributor.authorCooper, Mark Een
dc.contributor.authorGilbert, Richard Een
dc.date.accessioned2015-05-15T22:22:54Z
dc.date.available2015-05-15T22:22:54Z
dc.date.issued2001-08-01en
dc.identifier.citationKidney International; 60(2): 715-21en
dc.identifier.govdoc11473654en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/9325en
dc.description.abstractVasopeptidase inhibitors are a new class of cardiovascular compounds that inhibit both angiotensin-converting enzyme (ACE) and neutral endopeptidase (NEP). The aim of the present study was to explore the effects of omapatrilat, a vasopeptidase inhibitor, on renal function and pathology in subtotally nephrectomized (STNx) rats.STNx rats were randomized to four groups and treated for 12 weeks: no treatment (N = 14); omapatrilat at a low dose of 10 mg/kg (L, N = 12) and at a high dose of 40 mg/kg (H, N = 10); or an ACE inhibitor, fosinopril, at a dose of 10 mg/kg (N = 12). Sham-operated rats were used as control animals (N = 12).Elevated blood pressure in STNx rats (174 +/- 9 mm Hg) was reduced by omapatrilat in a dose-dependent manner (L, 121 +/- 3 mm Hg; H, 110 +/- 3 mm Hg) and by fosinopril (149 +/- 5 mm Hg). Proteinuria in STNx rats (246 +/- 73 mg/day) was reduced by treatment with fosinopril (88 +/- 21 mg/day) and was normalized by treatment with omapatrilat (L, 30 +/- 4 mg/day; H, 20 +/- 2 mg/day vs. control 25 +/- 1 mg/day). Decreased glomerular filtration rates, elevated plasma urea and creatinine and glomerulosclerosis, and tubulointerstitial fibrosis were ameliorated by omapatrilat and fosinopril to a similar degree. Compared with fosinopril, omapatrilat treatment was associated with increased plasma renin activity and decreased renal ACE and NEP binding in a dose-dependent manner.These findings suggest that vasopeptidase inhibition may provide a useful strategy for the treatment of progressive renal disease.en
dc.language.isoenen
dc.subject.otherAngiotensin-Converting Enzyme Inhibitors.pharmacologyen
dc.subject.otherAnimalsen
dc.subject.otherAutoradiographyen
dc.subject.otherBlood Pressure.drug effectsen
dc.subject.otherCreatinine.blooden
dc.subject.otherDisease Models, Animalen
dc.subject.otherFosinopril.pharmacologyen
dc.subject.otherGlomerular Filtration Rateen
dc.subject.otherHeart Failure.drug therapy.metabolismen
dc.subject.otherHypertension, Renal.drug therapy.metabolism.pathologyen
dc.subject.otherKidney.enzymologyen
dc.subject.otherMaleen
dc.subject.otherNephrectomyen
dc.subject.otherNeprilysin.analysis.antagonists & inhibitors.metabolismen
dc.subject.otherOrgan Sizeen
dc.subject.otherPeptidyl-Dipeptidase A.analysis.metabolismen
dc.subject.otherProteinuria.drug therapy.pathologyen
dc.subject.otherPyridines.pharmacologyen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherRenal Insufficiency.drug therapy.metabolism.pathologyen
dc.subject.otherRenin.blooden
dc.subject.otherThiazepines.pharmacologyen
dc.subject.otherUrea.blooden
dc.titleVasopeptidase inhibition attenuates the progression of renal injury in subtotal nephrectomized rats.en
dc.typeJournal Articleen
dc.identifier.journaltitleKidney internationalen
dc.identifier.affiliationUniversity of Melbourne Department of Medicine at Austin and Repatriation Medical Centre, Heidelberg West, Victoria, Australiaen
dc.identifier.affiliationcao@austin.unimelb.edu.auen
dc.identifier.doi10.1046/j.1523-1755.2001.060002715.xen
dc.description.pages715-21en
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pubmed/11473654en
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