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Ischemic injury in experimental stroke depends on angiotensin II

Item Type:Article
Title:Ischemic injury in experimental stroke depends on angiotensin II
Creators Name:Walther, T. and Olah, L. and Harms, C. and Maul, B. and Bader, M. and Hoertnagl, H. and Schultheiss, H.P. and Mies, G.
Abstract:Since pharmacological interactions of the renin-angiotensin system appear to alter the neurological outcome of stroke patients significantly, we examined the effect of elevated levels of angiotensin II and the role of its receptor subtype AT1 in brain infarction in transgenic mice after focal cerebral ischemia. Angiotensinogen-overexpressing and angiotensin receptor AT1 knockout mice underwent 1 h or 24 h permanent middle cerebral artery occlusion (MCAO). The current study revealed a much smaller penumbra size, i.e., brain tissue at risk, in angiotensinogen-overexpressing animals compared with their wild-type subgroup after 1 h MCAO, but an enlarged infarct size after 24 h. In contrast, a smaller lesion area of energy failure and a much larger penumbral area were found in AT1 knockout mice compared with wild-type littermates. Lower perfusion thresholds for ATP depletion and protein synthesis inhibition after MCAO in AT1-deficient mice and reduced cell damage in an in vitro model using embryonic neurons of AT1 knockout mice suggest injury mechanisms independent of arterial blood pressure. Our data, therefore, demonstrate a direct correlation between brain angiotensin II and the severity of ischemic injury in experimental stroke.
Keywords:A II, Focal cerebral ischemia, Transgenic mice, Penumbra, Collateral flow
Source:FASEB Journal
Publisher:Federation of American Societies for Experimental Biology
Page Range:169-176
Date:February 2002
Official Publication:https://doi.org/10.1096/fj.01-0601com
PubMed:View item in PubMed

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