Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1999-5-7
pubmed:abstractText
Thin filament regulation of contraction is thought to involve the binding of two activating ligands: Ca2+ and strongly bound cross-bridges. The specific cross-bridge states required to promote thin filament activation have not been identified. This study examines the relationship between cross-bridge cycling and thin filament activation by comparing the results of kinetic experiments using the Ca2+ sensitizers caffeine and bepridil. In single skinned rat soleus fibers, 30 mM caffeine produced a leftward shift in the tension-pCa relation from 6.03 +/- 0.03 to 6.51 +/- 0.03 pCa units and lowered the maximum tension to 0.60 +/- 0.01 of the control tension. In addition, the rate of tension redevelopment (ktr) was decreased from 3.51 +/- 0.12 s-1 to 2.70 +/- 0.19 s-1, and Vmax decreased from 1.24 +/- 0.07 to 0.64 +/- 0.02 M.L./s. Bepridil produced a similar shift in the tension-pCa curves but had no effect on the kinetics. Thus bepridil increases the Ca2+ sensitivity through direct effects on TnC, whereas caffeine has significant effects on the cross-bridge interaction. Interestingly, caffeine also produced a significant increase in stiffness under relaxing conditions (pCa 9.0), indicating that caffeine induces some strongly bound cross-bridges, even in the absence of Ca2+. The results are interpreted in terms of a model integrating cross-bridge cycling with a three-state thin-filament activation model. Significantly, strongly bound, non-tension-producing cross-bridges were essential to modeling of complete activation of the thin filament.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-1420891, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-1826677, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-2942677, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-2966401, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-3231093, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-3261996, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-3654633, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-3655718, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-3795099, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-4939977, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-6199685, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-6634380, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-7611352, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-7746802, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-7787068, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-7858135, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-7965829, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-8067434, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-8218897, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-8429546, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-8507667, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-8558467, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-8572183, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-8729701, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-8732507, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-8913615, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-9017207, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-9054965, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-9130449, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-9429160, http://linkedlifedata.com/resource/pubmed/commentcorrection/10096910-9525919
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0006-3495
pubmed:author
pubmed:issnType
Print
pubmed:volume
76
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2166-76
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Role of Ca2+ and cross-bridges in skeletal muscle thin filament activation probed with Ca2+ sensitizers.
pubmed:affiliation
Department of Physiology, University of Michigan, Ann Arbor, Michigan 48109-0622, USA. pwahr@umich.edu
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't