NDLI: Exaggeration of focal cerebral ischemia in transgenic mice carrying human Renin and human angiotensinogen genes.

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Exaggeration of focal cerebral ischemia in transgenic mice carrying human Renin and human angiotensinogen genes.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Senba, Izumi Kanno, Harumi Inaba, Shinji Tomono, Yumiko Iwai, Masaru Higaki, Jitsuo Horiuchi, Masatsugu Furuno, Megumi Okayama, Hideki Mogi, Masaki
Description	Country affiliation: Japan Author Affiliation: Inaba S ( Department of Molecular Cardiovascular Biology and Pharmacology, Ehime University Graduate School of Medicine, Shitsukawa, Tohon, Ehime, Japan.)
Abstract	BACKGROUND AND PURPOSE: We examined the possibility that activation of the human brain renin-angiotensin system is involved in enhancement of ischemic brain damage using chimeric transgenic mice with human renin (hRN) and human angiotensinogen (hANG) genes. METHODS: Chimeric (hRN/hANG-Tg) mice were generated by mating of hRN and hANG transgenic mice. Permanent occlusion of the middle cerebral artery (MCA) by an intraluminal filament technique induced focal ischemic brain lesions. RESULTS: hRN/hANG-Tg mice showed higher angiotensin II levels in the plasma and brain. The ischemic brain area at 24 hours after MCA occlusion was significantly enlarged in hRN/hANG-Tg mice with an enhanced neurological deficit compared to that in wild-type, hRN-Tg and hANG-Tg mice. The reduction of cerebral blood flow in the periphery region of the MCA territory after MCA occlusion was markedly exaggerated in hRN/hANG-Tg mice. Superoxide anion production in the brain and arteries was also increased significantly in hRN/hANG-Tg mice even before MCA occlusion and was further enhanced after MCA occlusion. Treatment with an AT(1) receptor blocker, valsartan (3.0 mg/kg per day), for 2 weeks significantly reduced the ischemic brain area and improved the neurological deficit after MCA occlusion in hRN/hANG-Tg mice, similar to those in wild-type, hRN-Tg, and hANG-Tg mice, with restoration of cerebral blood flow in the peripheral region and decreases in superoxide anion production and blood pressure. CONCLUSIONS: These results indicate that activation of the human renin-angiotensin system exaggerates ischemic brain damage mainly through stimulation of the AT(1) receptor and marked reduction of cerebral blood flow and enhanced oxidative stress.
ISSN	00392499
e-ISSN	15244628
Journal	Stroke
Issue Number	2
Volume Number	40
Language	English
Publisher	Lippincott Williams & Wilkins (on behalf of the American Heart Association)
Publisher Date	2009-02-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Angiotensinogen Genetics Brain Ischemia Pathology Renin Angiotensin Ii Metabolism Angiotensin Ii Type 1 Receptor Blockers Pharmacology Therapeutic Use Animals Brain Chemistry Physiology Drug Therapy Capillaries Cerebrovascular Circulation Infarction, Middle Cerebral Artery Mice Mice, Transgenic Oxidative Stress Receptor, Angiotensin, Type 1 Biosynthesis Receptor, Angiotensin, Type 2 Reverse Transcriptase Polymerase Chain Reaction Superoxides Tetrazoles Valine Analogs & Derivatives Valsartan Research Support, Non-u.s. Gov't Discipline Cardiology
Content Type	Text
Resource Type	Article
Subject	Cardiology and Cardiovascular Medicine Neuroscience Advanced and Specialized Nursing Neurology (clinical)

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