Abstract:
:Angiotensin II type 1 receptor (AT1R) blocker (ARB) has been reported to modify hypertensive cerebrovascular changes; however, it is not clear whether its protective effects are independent of blood pressure. The aim of this study was to clarify the role of AT1R-mediated signals in cerebral circulation by the chronic treatment with telmisartan, an ARB, at a dose that did not lower the blood pressure. Male spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY) were treated for 4 weeks from 16 weeks of ages with telmisartan (SHR-L: 0.3 mg/kg/day, SHR-H: 3 mg/kg/day, WKY-H: 3 mg/kg/day) or vehicle (SHR-V, WKY-V). Superoxide measured by a chemiluminescent assay or dihydroethidium fluorescence and vascular morphology were examined for the thoracic aorta (Ao), common carotid (CCA), middle cerebral (MCA) and basilar arteries (BA). After 4 weeks of treatment, the blood pressure significantly declined in SHR-H but not in SHR-L in comparison to SHR-V. The lower limit of cerebral blood flow (CBF) autoregulation, evaluated by hemorrhagic hypotension, was significantly lower in SHR-L and SHR-H than SHR-V. In both SHR and WKY, the superoxide levels in the arteries were significantly attenuated by both doses of ARB. ARB also reversed vascular hypertrophy in Ao, CCA and BA and the inward remodeling in MCA. These results suggest that chronic treatment with telmisartan may therefore improve CBF autoregulation with a restoration of the vascular structure and an attenuation of superoxide generation, even at a dose that does not lower the blood pressure.
journal_name
Exp Neuroljournal_title
Experimental neurologyauthors
Kumai Y,Ooboshi H,Ago T,Ishikawa E,Takada J,Kamouchi M,Kitazono T,Ibayashi S,Iida Mdoi
10.1016/j.expneurol.2007.11.028subject
Has Abstractpub_date
2008-04-01 00:00:00pages
441-8issue
2eissn
0014-4886issn
1090-2430pii
S0014-4886(07)00433-5journal_volume
210pub_type
杂志文章abstract::Chronic nerve compression (CNC) injuries induce a robust Schwann cell proliferation in a distinct spatial and temporal pattern, which is accompanied by an increase in the number of small un-myelinated axons in the area of the injury. These findings suggest that this local proliferation of Schwann cells may induce loca...
journal_title:Experimental neurology
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journal_title:Experimental neurology
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journal_title:Experimental neurology
pub_type: 杂志文章
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1006/exnr.2000.7572
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journal_title:Experimental neurology
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pub_type: 杂志文章,评审
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/j.expneurol.2003.07.006
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/0014-4886(91)90128-y
更新日期:1991-06-01 00:00:00
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/j.expneurol.2011.10.009
更新日期:2012-01-01 00:00:00
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journal_title:Experimental neurology
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doi:10.1016/0014-4886(89)90174-x
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1006/exnr.1998.6845
更新日期:1998-08-01 00:00:00
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pub_type: 杂志文章
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