Linked Life Data

11157672

Source:http://linkedlifedata.com/resource/pubmed/id/11157672

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-2-22
pubmed:abstractText
The aim of this study was to investigate how sarcoplasmic reticulum (SR) Ca(2+) content and systolic Ca(2+) are controlled when Ca(2+) entry into the cell is varied. Experiments were performed on voltage-clamped rat and ferret ventricular myocytes loaded with fluo-3 to measure intracellular Ca(2+) concentration ([Ca(2+)](i)). Increasing external Ca(2+) concentration ([Ca(2+)](o)) from 1 to 2 mmol/L increased the amplitude of the systolic Ca(2+) transient with no effect on SR Ca(2+) content. This constancy of SR content is shown to result because the larger Ca(2+) transient activates a larger Ca(2+) efflux from the cell that balances the increased influx. Decreasing [Ca(2+)](o) to 0.2 mmol/L decreased systolic Ca(2+) but produced a small increase of SR Ca(2+) content. This increase of SR Ca(2+) content is due to a decreased release of Ca(2+) from the SR resulting in decreased loss of Ca(2+) from the cell. An increase of [Ca(2+)](o) has two effects: (1) increasing the fraction of SR Ca(2+) content, which is released on depolarization and (2) increasing Ca(2+) entry into the cell. The results of this study show that the combination of these effects results in rapid changes in the amplitude of the systolic Ca(2+) transient. In support of this, the changes of amplitude of the transient occur more quickly following changes of [Ca(2+)](o) than following refilling of the SR after depletion with caffeine. We conclude that the coordinated control of increased Ca(2+) entry and greater fractional release of Ca(2+) is an important factor in regulating excitation-contraction coupling.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1524-4571
pubmed:author
pubmed:issnType
Electronic
pubmed:day
2
pubmed:volume
88
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
195-201
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11157672-4-Aminopyridine, pubmed-meshheading:11157672-Action Potentials, pubmed-meshheading:11157672-Aniline Compounds, pubmed-meshheading:11157672-Animals, pubmed-meshheading:11157672-Barium, pubmed-meshheading:11157672-Caffeine, pubmed-meshheading:11157672-Calcium, pubmed-meshheading:11157672-Calcium Channels, L-Type, pubmed-meshheading:11157672-Cells, Cultured, pubmed-meshheading:11157672-Electric Stimulation, pubmed-meshheading:11157672-Ferrets, pubmed-meshheading:11157672-Fluorescent Dyes, pubmed-meshheading:11157672-Intracellular Fluid, pubmed-meshheading:11157672-Myocardial Contraction, pubmed-meshheading:11157672-Patch-Clamp Techniques, pubmed-meshheading:11157672-Potassium Channel Blockers, pubmed-meshheading:11157672-Rats, pubmed-meshheading:11157672-Sarcoplasmic Reticulum, pubmed-meshheading:11157672-Sodium-Calcium Exchanger, pubmed-meshheading:11157672-Systole, pubmed-meshheading:11157672-Xanthenes
pubmed:year
2001
pubmed:articleTitle
Coordinated control of cell Ca(2+) loading and triggered release from the sarcoplasmic reticulum underlies the rapid inotropic response to increased L-type Ca(2+) current.
pubmed:affiliation
Unit of Cardiac Physiology, University of Manchester, Manchester, UK.trafford@man.ac.uk
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't