Document Detail


Selective effects of subarachnoid hemorrhage on cerebral vascular responses to 4-aminopyridine in rats.
MedLine Citation:
PMID:  11022080     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND AND PURPOSE: We postulated that some abnormalities in cerebrovascular function after subarachnoid hemorrhage (SAH) may involve underlying alterations in K(+) channel function. Thus, using pharmacological inhibitors, we assessed the influence of SAH on function of 2 types of K(+) channel in regulation of basilar artery diameter in vivo and membrane potential (E(m)) in vitro. METHODS: Rats were injected with saline (control) or autologous blood (SAH) into the cisterna magna. Two days later, effects of vasoactive drugs on the basilar artery were examined with a cranial window preparation. Vascular responses to 4-aminopyridine (4-AP), 3-aminopyridine (3-AP), tetraethylammonium (TEA), serotonin, acetylcholine, and adenosine were compared in control and SAH rats. Additional studies using intracellular microelectrodes evaluated the effects of 4-AP and serotonin on E(m) of basilar arteries isolated from control and SAH rats. RESULTS: Baseline artery diameter was 236+/-5 micrometer in control rats and 220+/-7 micrometer in SAH rats (P:<0. 05). 4-AP, but not 3-AP, constricted the basilar artery in control rats, and responses to 4-AP were reduced in SAH rats. Constrictor responses to TEA or serotonin were unaffected by SAH. Vasodilator responses to acetylcholine were impaired in SAH rats, whereas responses to adenosine were not different. Resting E(m) was -81+/-3 mV in control arteries and -79+/-3 mV in SAH arteries. Both 4-AP and serotonin depolarized the basilar artery, but only 4-AP-induced depolarization was impaired in SAH arteries. CONCLUSIONS: These data suggest that 4-AP induces cerebral vasoconstriction in vivo through smooth muscle depolarization due to inhibition of voltage-dependent K(+) channels. Furthermore, function of these K(+) channels may be selectively reduced in the basilar artery after SAH and thus could contribute to cerebral vascular dysfunction.
Authors:
L Quan; C G Sobey
Publication Detail:
Type:  In Vitro; Journal Article    
Journal Detail:
Title:  Stroke; a journal of cerebral circulation     Volume:  31     ISSN:  1524-4628     ISO Abbreviation:  Stroke     Publication Date:  2000 Oct 
Date Detail:
Created Date:  2000-10-13     Completed Date:  2000-10-26     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0235266     Medline TA:  Stroke     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  2460-5     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, University of Melbourne, Parkville, Victoria, Australia.
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MeSH Terms
Descriptor/Qualifier:
4-Aminopyridine / pharmacology*
Acetylcholine / metabolism,  pharmacology
Adenosine / metabolism,  pharmacology
Aminopyridines / pharmacology
Animals
Basilar Artery / drug effects,  metabolism
Blood Pressure / drug effects
Brain / blood supply*
Dose-Response Relationship, Drug
Male
Membrane Potentials / drug effects
Potassium Channel Blockers*
Potassium Channels / metabolism
Rats
Rats, Sprague-Dawley
Serotonin / metabolism,  pharmacology
Subarachnoid Hemorrhage / physiopathology*
Tetraethylammonium / pharmacology
Vasoconstriction / drug effects*
Vasodilation / drug effects*
Vasodilator Agents / pharmacology
Chemical
Reg. No./Substance:
0/Aminopyridines; 0/Potassium Channel Blockers; 0/Potassium Channels; 0/Vasodilator Agents; 462-08-8/3-aminopyridine; 50-67-9/Serotonin; 504-24-5/4-Aminopyridine; 51-84-3/Acetylcholine; 58-61-7/Adenosine; 66-40-0/Tetraethylammonium

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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