Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/10875
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dc.contributor.authorVelkoska, Elenaen
dc.contributor.authorDean, Rachael Gen
dc.contributor.authorBurchill, Luke Jen
dc.contributor.authorLevidiotis, Vickien
dc.contributor.authorBurrell, Louise Men
dc.date.accessioned2015-05-16T00:27:10Z
dc.date.available2015-05-16T00:27:10Z
dc.date.issued2010-02-01en
dc.identifier.citationClinical Science (london, England : 1979); 118(4): 269-79en
dc.identifier.govdoc19698082en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/10875en
dc.description.abstractAlterations within the RAS (renin-angiotensin system) are pivotal for the development of renal disease. ACE2 (angiotensin-converting enzyme 2) is expressed in the kidney and converts the vasoconstrictor AngII (angiotensin II) into Ang-(1-7), a peptide with vasodilatory and anti-fibrotic actions. Although the expression of ACE2 in the diabetic kidney has been well studied, little is known about its expression in non-diabetic renal disease. In the present study, we assessed ACE2 in rats with acute kidney injury induced by STNx (subtotal nephrectomy). STNx and Control rats received vehicle or ramipril (1 mg. kg (-1) of body weight . day (-1), and renal ACE, ACE2 and mas receptor gene and protein expression were measured 10 days later. STNx rats were characterized by polyuria, proteinuria, hypertension and elevated plasma ACE2 activity (all P<0.01) and plasma Ang-(1-7) (P<0.05) compared with Control rats. There was increased cortical ACE binding and medullary mas receptor expression (P<0.05), but reduced cortical and medullary ACE2 activity in the remnant kidney (P<0.05 and P<0.001 respectively) compared with Control rats. In STNx rats, ramipril reduced blood pressure (P<0.01), polyuria (P<0.05)and plasma ACE2 (P<0.01), increased plasma Ang-(1-7) (P<0.001), and inhibited renal ACE(P<0.001). Ramipril increased both cortical and medullary ACE2 activity (P<0.01), but reduced medullary mas receptor expression (P<0.05). In conclusion, our results show that ACE2 activity is reduced in kidney injury and that ACE inhibition produced beneficial effects in association with increased renal ACE2 activity. As ACE2 both degrades AngII and generates the vasodilator Ang-(1-7), a decrease in renal ACE2 activity, as observed in the present study, has the potential to contribute to the progression of kidney disease.en
dc.language.isoenen
dc.subject.otherAngiotensin-Converting Enzyme Inhibitors.pharmacologyen
dc.subject.otherAnimalsen
dc.subject.otherFemaleen
dc.subject.otherGene Expressionen
dc.subject.otherHypertension.drug therapy.metabolismen
dc.subject.otherKidney.drug effects.injuries.metabolismen
dc.subject.otherNephrectomyen
dc.subject.otherPeptidyl-Dipeptidase A.metabolismen
dc.subject.otherPolyuria.drug therapy.metabolismen
dc.subject.otherProteinuria.drug therapy.metabolismen
dc.subject.otherProto-Oncogene Proteins.genetics.metabolismen
dc.subject.otherRamipril.pharmacologyen
dc.subject.otherRandom Allocationen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherReceptors, G-Protein-Coupled.genetics.metabolismen
dc.titleReduction in renal ACE2 expression in subtotal nephrectomy in rats is ameliorated with ACE inhibition.en
dc.typeJournal Articleen
dc.identifier.journaltitleClinical science (London, England : 1979)en
dc.identifier.affiliationDepartment of Medicine, The University of Melbourne, Austin Health, Heidelberg 3081, Victoria, Australiaen
dc.identifier.doi10.1042/CS20090318en
dc.description.pages269-79en
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pubmed/19698082en
Appears in Collections:Journal articles

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