Document Detail


Extracellular K(+)-induced hyperpolarizations and dilatations of rat coronary and cerebral arteries involve inward rectifier K(+) channels.
MedLine Citation:
PMID:  9019539     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
1. The hypothesis that inward rectifier K(+) channels are involved in the vasodilatation of small coronary and cerebral arteries (100-200 microm diameter) in response to elevated [K+]o was tested. The diameters and membrane potentials of pressurized arteries from rat were measured using a video-imaging system and conventional microelectrodes, respectively. 2. Elevation of [K+]o from 6 to 16 mM caused the membrane potential of pressurized (60 mmHg) arteries to hyperpolarize by 12-14 mV. Extracellular Ba(2+) (Ba2+(o)) blocked K(+)-induced membrane potential hyperpolarizations at concentrations (IC(50), 6 microM) that block inward rectifier K(+) currents in smooth muscle cells isolated from these arteries. 3. Elevation of [K+]o from 6 to 16 mM caused sustained dilatations of pressurized coronary and cerebral arteries with diameters increasing from 125 to 192 microm and 110 to 180 microm in coronary and cerebral arteries, respectively. Ba2+(o) blocked K(+)-induced dilatations of pressurized coronary and cerebral arteries (IC50, 3-8 microM). 4. Elevated [K+]o-induced vasodilatation was not prevented by blockers of other types of K(+) channels (1 mM 4-aminopyridine, 1 mM TEA+, and 10 mu M glibenclamide), and blockers of Na(+)-K(+)-ATPase. Elevated [K+]o-induced vasodilatation was unaffected by removal of the endothelium. 5. These findings suggest that K+(o) dilates small rat coronary and cerebral arteries through activation of inward rectifier K(+) channels. Furthermore, these results support the hypothesis that inward rectifier K(+) channels may be involved in metabolic regulation of coronary and cerebral blood flow in response to changes in [K+]o.
Authors:
H J Knot; P A Zimmermann; M T Nelson
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of physiology     Volume:  492 ( Pt 2)     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  1996 Apr 
Date Detail:
Created Date:  1997-02-11     Completed Date:  1997-02-11     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  419-30     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, University of Vermont, Colchester, VT 05446-2500, USA. knot@northpole.med.uvm.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Arteries / drug effects,  physiology
Barium / pharmacology
Cerebral Arteries / drug effects,  physiology*
Coronary Vessels / drug effects,  physiology*
Electrophysiology
Endothelium, Vascular / physiology
Extracellular Space / metabolism*
Female
Potassium / physiology*
Potassium Channel Blockers
Potassium Channels / physiology*
Rats
Rats, Sprague-Dawley
Sodium-Potassium-Exchanging ATPase / antagonists & inhibitors
Vasodilation* / drug effects
Grant Support
ID/Acronym/Agency:
HL-44455/HL/NHLBI NIH HHS; HL-51728/HL/NHLBI NIH HHS; HL-67647/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Potassium Channel Blockers; 0/Potassium Channels; 7440-09-7/Potassium; 7440-39-3/Barium; EC 3.6.3.9/Sodium-Potassium-Exchanging ATPase
Comments/Corrections

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


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