Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/13636
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dc.contributor.authorCooper, Mark Een
dc.contributor.authorCao, Zeminen
dc.contributor.authorRumble, J Ren
dc.contributor.authorJandeleit, Ken
dc.contributor.authorAllen, Terri Jen
dc.contributor.authorGilbert, Richard Een
dc.date.accessioned2015-05-16T03:31:18Z
dc.date.available2015-05-16T03:31:18Z
dc.date.issued1998-12-01en
dc.identifier.citationMetabolism: Clinical and Experimental; 47(12 Suppl 1): 24-7en
dc.identifier.govdoc9867067en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/13636en
dc.description.abstractVascular disease is now the major cause of morbidity and mortality in the diabetic population. Our group explored the vascular changes associated with experimental diabetes and examined whether these changes can be ameliorated by angiotensin-converting enzyme (ACE) inhibition. The ACE inhibitor perindopril (PE) was administered to streptozotocin-induced diabetic rats for 24 weeks. At death, mesenteric vessels were perfused in vivo followed by assessment of the vascular architecture by quantitative histomorphometry. In a subgroup of animals, RNA was extracted from the mesenteric vasculature for assessment of gene expression of the prosclerotic cytokine, transforming growth factor beta 1 (TGFbeta1), and the matrix protein, type IV collagen. Diabetes was associated with smooth muscle hypertrophy and extracellular matrix (ECM) accumulation. ECM accumulation, particularly collagen deposition, was observed in the medial and adventitial layers. ACE inhibition prevented mesenteric vascular hypertrophy after 24 weeks of diabetes. In addition, overexpression of TGFbeta1 in the vessels of diabetic animals was prevented by PE treatment. Similarly, type IV collagen mRNA levels were increased in diabetic vessels, and this overexpression was also prevented by PE therapy. In summary, ACE inhibition attenuates many of the vascular changes observed in experimental diabetes and may have important clinical implications as a vasoprotective agent in human diabetes.en
dc.language.isoenen
dc.subject.otherAngiotensin-Converting Enzyme Inhibitors.therapeutic useen
dc.subject.otherAnimalsen
dc.subject.otherBlood Vessels.pathologyen
dc.subject.otherDiabetes Mellitus, Experimental.drug therapy.genetics.pathologyen
dc.subject.otherDiabetic Angiopathies.drug therapy.genetics.pathologyen
dc.subject.otherHypertrophyen
dc.subject.otherIndoles.therapeutic useen
dc.subject.otherMaleen
dc.subject.otherPerindoprilen
dc.subject.otherRNA, Messenger.metabolismen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherSplanchnic Circulation.drug effectsen
dc.subject.otherTransforming Growth Factor beta.geneticsen
dc.titleAttenuation of diabetes-associated mesenteric vascular hypertrophy with perindopril: morphological and molecular biological studies.en
dc.typeJournal Articleen
dc.identifier.journaltitleMetabolism: clinical and experimentalen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin & Repatriation Medical Centre, Heidelberg, Victoria, Australiaen
dc.description.pages24-7en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/9867067en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.languageiso639-1en-
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