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Renal ischemia reperfusion injury increases renal generation of angiotensin Ⅱ (Ang Ⅱ) which could worsen renal vasocontraction.Thus, we investigated the hypothesis that renal ischemia reperfusion injury alters renal afferent arteriolar responses to Ang Ⅱ via production of hydrogen peroxide (H2O2), or superoxide (O2) or via altered angiotensin type 1 receptor (AT1R) expression.Afferent arterioles of mouse kidneys 24h after renal ischemia reperfusion or sham procedures were isolated and perfused.Responses to Ang Ⅱ or norepinephrine (NE) were assessed by measurement of arteriolar luminal diameter.The mRNA expressions of AT1 receptor (AT1R) and AT2 receptor (AT2R) were evaluated by quantificational realtime polymerase chain reaction.Compared to sham group,afferent arterioles from mouse kidneys after renal ischemia reperfusion had impaired contractions to Ang Ⅱ (4.63± 3.06) % versus (29.95 ± 1.31) % at 109 mol · L1, P < 0.05, (27.07± 1.50) % versus (41.74±0.60)% at 107 mol · L1, P <0.05) that were normalized by incubation with PEGcatalase, but unaffected by PEGSOD.However, the NE responses of afferent arterioles after renal ischemia reperfusion were unchanged.Compared to the sham group, renal ischemia reperfusion significantly increased the renal cortical H2O2 (0.123 ±0.006) versus (0.087 ± 0.003) mmol · g1 protein, P < 0.01), reduced catalase activity 〔 (14.81 ± 3.22) versus (28.49 ± 1.62) units ·mg1 protein, P < 0.01 〕 and downregulated mRNA for AT1R (0.27± 0.02 versus0.95 ± 0.02, P < 0.01).We conclude that afferent arteriolar responses to Ang Ⅱ are impaired selectively in mice after renal ischemia reperfusion by accumulation of H2O2 and reduced expression of AT1R.