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Increased hydrogen peroxide impairs angiotensin II contractions of afferent arterioles in mice after renal ischaemia-reperfusion injury
Zhejiang Univ, Dept Physiol, Sch Med, Hangzhou 310058, Zhejiang, Peoples R China..
Zhejiang Univ, Dept Physiol, Sch Med, Hangzhou 310058, Zhejiang, Peoples R China..
Zhejiang Univ, Dept Physiol, Sch Med, Hangzhou 310058, Zhejiang, Peoples R China..
Zhejiang Univ, Dept Physiol, Sch Med, Hangzhou 310058, Zhejiang, Peoples R China..
Vise andre og tillknytning
2016 (engelsk)Inngår i: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 218, nr 2, 136-145 s.Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

AimRenal ischaemia-reperfusion injury (IRI) increases angiotensin II (Ang II) and reactive oxygen species (ROS) that are potent modulators of vascular function. However, the roles of individual ROS and their interaction with Ang II are not clear. Here we tested the hypothesis that IRI modulates renal afferent arteriolar responses to Ang II via increasing superoxide (O2-) or hydrogen peroxide (H2O2). MethodsRenal afferent arterioles were isolated and perfused from C57BL/6 mice 24h after IRI or sham surgery. Responses to Ang II or noradrenaline were assessed by measuring arteriolar diameter. Production of H2O2 and O2-was assessed in afferent arterioles and renal cortex. Activity of SOD and catalase, and mRNA expressions of Ang II receptors were assessed in pre-glomerular arterioles and renal cortex. ResultsAfferent arterioles from mice after IRI had a reduced maximal contraction to Ang II (-272 vs. -42 +/- 1%, P<0.001), but retained a normal contraction to noradrenaline. Arterioles after IRI had a 38% increase in H2O2 (P<0.001) and a 45% decrease in catalase activity (P<0.01). Contractions were reduced in normal arterioles after incubation with H2O2 (-22 +/- 2 vs. -42 +/- 1%, P<0.05) similar to the effects of IRI. However, the impaired contractions were normalized by incubation with PEG catalase despite a reduced AT(1)R expression. ConclusionsRenal IRI in mice selectively impairs afferent arteriolar responses to Ang II because of H2O2 accumulation that is caused by a reduced catalase activity(.) This could serve to buffer the effect of Ang II after IRI and may be a protective mechanism.

sted, utgiver, år, opplag, sider
2016. Vol. 218, nr 2, 136-145 s.
Emneord [en]
afferent arteriole, angiotensin II, catalase, hydrogen peroxide, ischaemia-reperfusion injury
HSV kategori
Identifikatorer
URN: urn:nbn:se:uu:diva-307716DOI: 10.1111/apha.12745ISI: 000383576900011PubMedID: 27362287OAI: oai:DiVA.org:uu-307716DiVA: diva2:1048603
Tilgjengelig fra: 2016-11-21 Laget: 2016-11-21 Sist oppdatert: 2016-11-21bibliografisk kontrollert

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