| Oxyhemoglobin-induced expression of R-type Ca2+ channels in cerebral arteries. | |
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MedLine Citation:
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PMID: 18436877 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND AND PURPOSE: Cerebral vasospasm after subarachnoid hemorrhage (SAH) is a major contributor to mortality and morbidity after aneurysm rupture. Recently, R-type voltage-dependent Ca(2+) channel (VDCC) expression has been associated with increased cerebral artery constriction in a rabbit model of SAH. The goal of the present study was to examine whether the blood component oxyhemoglobin (oxyHb) can mimic the ability of SAH to cause R-type VDCC expression in the cerebral vasculature. METHODS: Rabbit cerebral arteries were organ cultured in serum-free media for up to 5 days in the presence or absence of purified oxyHb (10 micromol/L). Diameter changes in response to diltiazem, (L-type VDCC antagonist) and SNX-482 (R-type VDCC antagonist) were recorded at day 1, 3, or 5 in arteries constricted by elevated extracellular potassium. RT-PCR was performed on RNA extracted from arteries cultured for 5 days (+/-oxyHb) to assess VDCC expression. RESULTS: After 5 days, oxyHb-treated arteries were less sensitive and partially resistant to diltiazem compared to similar arteries organ cultured in the absence of oxyHb. Further, SNX-482 dilated arteries organ cultured for 5 days in the presence, but not in the absence, of oxyHb. RT-PCR revealed that oxyHb treated arteries expressed R-type VDCCs (Ca(V) 2.3) in addition to L-type VDCCs (Ca(V) 1.2), whereas untreated arteries expressed only Ca(V) 1.2. CONCLUSIONS: These results demonstrate that oxyhemoglobin exposure for 5 days induces the expression of Ca(V) 2.3 in cerebral arteries. We propose that oxyhemoglobin contributes to enhanced cerebral artery constriction after SAH via the emergence of R-type VDCCs. |
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Authors:
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Timothy E Link; Kentaro Murakami; Micah Beem-Miller; Bruce I Tranmer; George C Wellman |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2008-04-24 |
Journal Detail:
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Title: Stroke; a journal of cerebral circulation Volume: 39 ISSN: 1524-4628 ISO Abbreviation: Stroke Publication Date: 2008 Jul |
Date Detail:
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Created Date: 2008-06-24 Completed Date: 2008-07-23 Revised Date: 2009-11-18 |
Medline Journal Info:
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Nlm Unique ID: 0235266 Medline TA: Stroke Country: United States |
Other Details:
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Languages: eng Pagination: 2122-8 Citation Subset: IM |
Affiliation:
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Department of Pharmacology, University of Vermont College of Medicine, 86 Beaumont Ave, Burlington, VT 05405, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Aneurysm
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metabolism Animals Calcium Channel Blockers / pharmacology Calcium Channels / metabolism* Cerebral Arteries / metabolism* Culture Media, Serum-Free / pharmacology Diltiazem / pharmacology Endothelium, Vascular / metabolism Gene Expression Regulation* Male Muscle, Smooth / metabolism Oxyhemoglobins / biosynthesis* Rabbits Subarachnoid Hemorrhage / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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P20 RR016435-060005/RR/NCRR NIH HHS; P20 RR16435/RR/NCRR NIH HHS; R01 HL078983/HL/NHLBI NIH HHS; R01 HL078983-02/HL/NHLBI NIH HHS; R01 HL078983-03/HL/NHLBI NIH HHS; R01 HL078983-04/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Calcium Channel Blockers; 0/Calcium Channels; 0/Culture Media, Serum-Free; 0/Oxyhemoglobins; 42399-41-7/Diltiazem |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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