Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/13634
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dc.contributor.authorRumble, J Ren
dc.contributor.authorGilbert, Richard Een
dc.contributor.authorCox, Allison Jen
dc.contributor.authorWu, Len
dc.contributor.authorCooper, Mark Een
dc.date.accessioned2015-05-16T03:31:17Z
dc.date.available2015-05-16T03:31:17Z
dc.date.issued1998-11-01en
dc.identifier.citationJournal of Hypertension; 16(11): 1603-9en
dc.identifier.govdoc9856360en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/13634en
dc.description.abstractThe purpose of this study was to assess the role of transforming growth factor (TGF)-beta1 in the development of diabetes-associated mesenteric vascular hypertrophy and in the antitrophic effect of angiotensin converting enzyme inhibitors.Streptozotocin-induced diabetic and control Sprague-Dawley rats were randomly allocated to treatment with the angiotensin converting enzyme inhibitor ramipril or to no treatment and were killed 1 or 3 weeks after the streptozotocin injection. Blood was collected and mesenteric vessels removed. Mesenteric vascular weight was measured and TGF-beta1 and alpha1 (type IV) collagen messenger (m)RNA levels were analysed by Northern analysis. Immunohistochemical analyses for TGF-beta1 and type IV collagen were also performed.The diabetic rats had increased mesenteric vessel weight at 3 weeks but not at 1 week and a concomitant rise in mesenteric TGF-beta1 and in alpha1 (type IV) collagen mRNA levels. Ramipril treatment attenuated mesenteric vessel hypertrophy and prevented the increase in TGF-beta1 and alpha1 (type IV) collagen mRNA levels after 3 weeks of diabetes. The immunohistochemical analysis revealed that diabetes was associated with increased TGF-beta1 and type IV collagen protein and extracellular matrix accumulation in mesenteric vessels, and this increase was reduced by ramipril treatment.These results support the concept that TGF-beta is involved in the changes associated with diabetic vascular disease, and suggest a mechanism by which angiotensin converting enzyme inhibitors exert their antitrophic effects.en
dc.language.isoenen
dc.subject.otherAngiotensin-Converting Enzyme Inhibitors.pharmacologyen
dc.subject.otherAnimalsen
dc.subject.otherBlood Glucose.drug effectsen
dc.subject.otherBlood Pressure.drug effectsen
dc.subject.otherBlotting, Northernen
dc.subject.otherBody Weight.drug effectsen
dc.subject.otherCollagen.geneticsen
dc.subject.otherDiabetes Mellitus, Experimental.complicationsen
dc.subject.otherDiabetic Angiopathies.complications.genetics.metabolismen
dc.subject.otherGene Expression.drug effectsen
dc.subject.otherImmunohistochemistryen
dc.subject.otherMaleen
dc.subject.otherRNA, Messenger.analysis.geneticsen
dc.subject.otherRamipril.pharmacologyen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherTransforming Growth Factor beta.geneticsen
dc.subject.otherVascular Diseases.complications.genetics.metabolismen
dc.titleAngiotensin converting enzyme inhibition reduces the expression of transforming growth factor-beta1 and type IV collagen in diabetic vasculopathy.en
dc.typeJournal Articleen
dc.identifier.journaltitleJournal of Hypertensionen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin & Repatriation Medical Centre, Heidelberg, Australiaen
dc.description.pages1603-9en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/9856360en
dc.type.austinJournal Articleen
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en-
item.openairetypeJournal Article-
item.grantfulltextnone-
item.cerifentitytypePublications-
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