Abstract:
:Rationale exists for suspecting that angiotensin (Ang) and arginine vasopressin (AVP) given by the intracerebroventricular (IVT) route can affect cerebrospinal fluid (CSF) pressure. This hypothesis was tested in conscious, unrestrained adult male Sprague-Dawley rats with IVT and left carotid arterial catheters. The rats were infused (IVT) for 30 min with artificial CSF followed by 30 additional minutes with CSF, Ang, (0.6 micrograms/h) AVP (5 or 50 ng/h), or AVP (5 or 50 ng/h) + Ang, (0.6 micrograms/h). Angiotensin evoked a central hypertensive effect (+ 16 mm Hg) and increased CSF pressure from 10 to 16 cm H2O (P less than 0.05). Neither dose of AVP affected blood or CSF pressures. The AVP (5 ng/h) prevented Ang-induced changes in blood and CSF pressures and AVP (50 ng/h) blocked only the Ang-induced rise in CSF pressure. These results raise the possibility that angiotensin and vasopressin participate in the regulation of CSF pressure.
journal_name
Exp Neuroljournal_title
Experimental neurologyauthors
Barbella YR,Keil LC,Wurpel JN,Severs WBdoi
10.1016/0014-4886(83)90405-3subject
Has Abstractpub_date
1983-11-01 00:00:00pages
325-34issue
2eissn
0014-4886issn
1090-2430journal_volume
82pub_type
杂志文章abstract::One of the primary hallmarks of glutamate excitotoxicity is degradation of the neuronal cytoskeleton. Using a tissue culture approach, we have investigated the relationship between excitotoxicity and cytoskeletal degradation within axons, with particular reference to the axon specific neurofilament proteins. Neurofila...
journal_title:Experimental neurology
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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
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journal_title:Experimental neurology
pub_type: 杂志文章,评审
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/0014-4886(83)90328-x
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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:10.1016/0014-4886(91)90007-y
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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
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pub_type: 杂志文章
doi:10.1006/exnr.1993.1050
更新日期:1993-04-01 00:00:00
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journal_title:Experimental neurology
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更新日期:2006-02-01 00:00:00
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/0014-4886(87)90244-5
更新日期:1987-11-01 00:00:00
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journal_title:Experimental neurology
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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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更新日期:1995-06-01 00:00:00
abstract::Tamoxifen-induced mutagenesis via the so-called CreER(T2) fusion enzyme is a key technology for the inducible gene knockout in the adult murine brain. However, it requires a subchronic transient treatment with high doses of the non-selective estrogen receptor antagonist tamoxifen. It has been shown earlier that acute ...
journal_title:Experimental neurology
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更新日期:2008-05-01 00:00:00
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journal_title:Experimental neurology
pub_type: 杂志文章
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更新日期:1990-12-01 00:00:00
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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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更新日期:1989-09-01 00:00:00