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出 处:《中国药理学通报》2015年第B11期98-98,共1页Chinese Pharmacological Bulletin
摘 要:Renal ischemia reperfusion injury increases renal generation of angiotensin II (Ang Ⅱ) which could wors- en renal vasocontraction. Thus, we investigated the hypothesis that renal ischemia reperfusion injury alters renal af- ferent arteriolar responses to Ang II via production of hydrogen peroxide ( H202 ), or superoxide ( O2 ) or via al- tered angiotensin type 1 receptor (AT1R) expression. Afferent arterioles of mouse kidneys 24h after renal ischemia repeffusion or sham procedures were isolated and perfused. Responses to Ang II or norepinephrine (NE) were as- sessed by measurement of arteriolar luminal diameter. The mRNA expressions of AT1 receptor ( AT1 R) and AT2 re- ceptor (ATzR) were evaluated by quantificational real-time 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 10 -9 tool · ^-1, p 〈 0.05 , ( - 27.07 ± 1 50) % versus ( - 41 74 ± 0.60) % at 10^-7 tool · L^-1, P 〈 0.05 ) that were normalized by incubation with PEG-catalase , but unaffected by PEG-SOD. However, the NE responses of afferent arterioles after renal ischemia reperfusion were unchanged. Com- pared to the sham group, renal ischemia reperfusion significantly increased the renal cortical H202 (0. 123 ± -1 0. 006) versus (0. 087 ± 0. 003) mmol·mg protein, P 〈 0.01 ), reduced catalase activity [ ( 14.81 ± 3.22) ver- sus (28.49 ± 1.62) units · mg^-1 protein, P 〈 0.01 ] and downregulated mRNA for AT1R (0.27 ± 0.02 versus 0.95 ± 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 H202 and reduced expression of AT1R.
关 键 词:ANGIOTENSIN ISCHEMIA NOREPINEPHRINE receptor procedures protein H202 AT1R
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