Linked Life Data

9683429

Source:http://linkedlifedata.com/resource/pubmed/id/9683429

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2 Pt 2
pubmed:dateCreated
1998-9-16
pubmed:abstractText
The effect of Cs+ on the function of the cardiac sarcoplasmic reticulum (SR) has been investigated in skinned cardiac myocytes. Isolated rat ventricular myocytes were permeabilized using saponin and then perfused with a solution containing 150 nmol/l Ca2+ and 10 micromol/l fura 2. Fura 2 fluorescence from the skinned cell was monitored to assess SR Ca2+ release. The frequency of spontaneous Ca2+ release from the SR decreased when K+ in the bathing solution was completely replaced with Cs+. Cs+ had little effect on the amplitude of spontaneous release but prolonged both the rise time and decay time. The SR Ca2+ content, assessed by application of caffeine, was reduced in the Cs+ solution. Cyclopiazonic acid produced effects similar to those of Cs+. Extracellular Cs+ (20 mmol/l) increased the amplitude of the Ca2+ transient and the SR Ca2+ content in intact field-stimulated cells but had little effect on the Ca2+ transient when the amplitude and duration of depolarization were kept constant using voltage clamp. These data suggest that Cs+ slows Ca2+ movement across the SR membrane, possibly by blocking the SR K+ channel, but has additional effects in intact cells that overcome its inhibitory effects on the SR.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
275
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H422-30
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Cs+ inhibits spontaneous Ca2+ release from sarcoplasmic reticulum of skinned cardiac myocytes.
pubmed:affiliation
Department of Physiology, University of Leeds, Leeds LS2 9NQ, United Kingdom.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't