Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9266
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dc.contributor.authorCao, Zeminen
dc.contributor.authorCooper, Mark Een
dc.contributor.authorWu, L Len
dc.contributor.authorCox, Allison Jen
dc.contributor.authorJandeleit-Dahm, Ken
dc.contributor.authorKelly, D Jen
dc.contributor.authorGilbert, Richard Een
dc.date.accessioned2015-05-15T22:17:34Z
dc.date.available2015-05-15T22:17:34Z
dc.date.issued2000-10-01en
dc.identifier.citationHypertension; 36(4): 561-8en
dc.identifier.govdoc11040236en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/9266en
dc.description.abstractThe renin-angiotensin system (RAS) and endothelin system may both play a role in the pathogenesis of progressive renal injury. The aims of the present study were 3-fold: first, to explore the possible benefits of dual blockade of the RAS with an ACE inhibitor and an angiotensin type 1(AT1) receptor antagonist; second, to examine the relative efficacy of endothelin A receptor antagonism (ETA-RA) compared with combined endothelin A/B receptor antagonism (ETA/B-RA); and third, to assess whether interruption of both RAS and endothelin system had any advantages over single-system blockade. Subtotally nephrectomized rats were studied as a model of progressive renal injury and randomly assigned to one of the following treatments for 12 weeks: perindopril (ACE inhibitor), irbesartan (AT1 receptor antagonist), BMS193884 (ETA-RA), bosentan (ETA/B-RA), and a combination of irbesartan with either perindopril or BMS193884. Treatment with irbesartan or perindopril was associated with an improved glomerular filtration rate and reductions in blood pressure, urinary protein excretion, glomerulosclerosis, and tubular injury in association with reduced gene expression of transforming growth factor-beta(1) and matrix protein type IV collagen. The combination of irbesartan with perindopril was associated with further reductions in blood pressure and urinary protein excretion. No beneficial effects of either BMS193884 or bosentan were noted. Furthermore, the addition of BMS193884 to irbesartan did not confer any additional benefits. These findings suggest that the RAS but not the endothelin system is a major mediator of progressive renal injury after renal mass reduction and that the combination of an AT1 receptor antagonist with an ACE inhibitor may have advantages over the single agent of RAS blocker treatment.en
dc.language.isoenen
dc.subject.otherAngiotensin Receptor Antagonistsen
dc.subject.otherAngiotensin-Converting Enzyme Inhibitors.administration & dosageen
dc.subject.otherAnimalsen
dc.subject.otherAntihypertensive Agents.administration & dosageen
dc.subject.otherBlood Pressure.drug effectsen
dc.subject.otherCollagen.genetics.metabolismen
dc.subject.otherDisease Models, Animalen
dc.subject.otherDisease Progressionen
dc.subject.otherDrug Therapy, Combinationen
dc.subject.otherEndothelin Receptor Antagonistsen
dc.subject.otherEndothelin-1.metabolismen
dc.subject.otherGlomerular Filtration Rate.drug effectsen
dc.subject.otherKidney.drug effects.metabolism.pathologyen
dc.subject.otherMaleen
dc.subject.otherNephrectomyen
dc.subject.otherProteinuria.urineen
dc.subject.otherRNA, Messenger.metabolismen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherReceptor, Angiotensin, Type 1en
dc.subject.otherReceptor, Angiotensin, Type 2en
dc.subject.otherReceptor, Endothelin Aen
dc.subject.otherReceptor, Endothelin Ben
dc.subject.otherRenal Insufficiency.drug therapy.metabolismen
dc.subject.otherRenin-Angiotensin System.drug effectsen
dc.subject.otherSeverity of Illness Indexen
dc.subject.otherTransforming Growth Factor beta.genetics.metabolismen
dc.titleBlockade of the renin-angiotensin and endothelin systems on progressive renal injury.en
dc.typeJournal Articleen
dc.identifier.journaltitleHypertensionen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin and Repatriation Medical Centre, Heidelberg West, Victoria, Australiaen
dc.description.pages561-8en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/11040236en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
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