Linked Life Data

7694496

Source:http://linkedlifedata.com/resource/pubmed/id/7694496

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5 Pt 1
pubmed:dateCreated
1993-12-22
pubmed:abstractText
Inward rectifier K+ channels have been implicated in the control of membrane potential and external K(+)-induced dilations of small cerebral arteries. In the present study, whole cell K+ currents through the inward rectifier K+ channel were measured in single smooth muscle cells isolated from the posterior cerebral artery of Wistar-Kyoto rats. The whole cell K+ current-voltage relationship showed inward rectification. Inward currents were recorded negative to the K+ equilibrium potential, whereas outward currents were small. When extracellular K+ was elevated, the zero current potential shifted to the new K+ equilibrium potential, and the conductance of the inward current increased. Inward currents were reduced by external barium or cesium. Inhibition by barium and cesium increased with membrane hyperpolarization. The half-inhibition constant for barium was 2.2 microM at -60 mV, increasing e-fold for a 23-mV depolarization. We provide the first direct measurements of inward rectifier K+ currents in single smooth muscle cells and show that external barium ions are effective blockers of these currents.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
265
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
C1363-70
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Inward rectifier K+ currents in smooth muscle cells from rat resistance-sized cerebral arteries.
pubmed:affiliation
Department of Pharmacology, Medical Research Facility, University of Vermont, Colchester 05446.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't