Physiology Cambridge Electronic Design Limited
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Physiology 22: 73-80, 2007; doi:10.1152/physiol.00043.2006
1548-9213/07 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (8)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hinken, A. C.
Right arrow Articles by Solaro, R. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hinken, A. C.
Right arrow Articles by Solaro, R. J.
Physiology, Vol. 22, No. 2, 73-80, April 2007
© 2007 Int. Union Physiol. Sci./Am. Physiol. Soc.

REVIEW

A Dominant Role of Cardiac Molecular Motors in the Intrinsic Regulation of Ventricular Ejection and Relaxation

Aaron C. Hinken and R. John Solaro

Department of Physiology and Biophysics and Center for Cardiovascular Research, College of Medicine, University of Illinois at Chicago, Illinois solarorj{at}uic.edu

Molecular motors housed in myosins of the thick filament react with thin-filament actins and promote force and shortening in the sarcomeres. However, other actions of these motors sustain sarcomeric activation by cooperative feedback mechanisms in which the actin-myosin interaction promotes thin-filament activation. Mechanical feedback also affects the actin-myosin interaction. We discuss current concepts of how these relatively under-appreciated actions of molecular motors are responsible for modulation of the ejection time and isovolumic relaxation in the beating heart.




This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
R. J. Solaro
Multiplex Kinase Signaling Modifies Cardiac Function at the Level of Sarcomeric Proteins
J. Biol. Chem., October 3, 2008; 283(40): 26829 - 26833.
[Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
K. B. Campbell, A. M. Simpson, S. G. Campbell, H. L. Granzier, and B. K. Slinker
Dynamic left ventricular elastance: a model for integrating cardiac muscle contraction into ventricular pressure-volume relationships
J Appl Physiol, April 1, 2008; 104(4): 958 - 975.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
B. Iorga, N. Blaudeck, J. Solzin, A. Neulen, I. Stehle, A. J. L. Davila, G. Pfitzer, and R. Stehle
Lys184 deletion in troponin I impairs relaxation kinetics and induces hypercontractility in murine cardiac myofibrils
Cardiovasc Res, March 1, 2008; 77(4): 676 - 686.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Biol. CellHome page
A. Cammarato, C. M. Dambacher, A. F. Knowles, W. A. Kronert, R. Bodmer, K. Ocorr, and S. I. Bernstein
Myosin Transducer Mutations Differentially Affect Motor Function, Myofibril Structure, and the Performance of Skeletal and Cardiac Muscles
Mol. Biol. Cell, February 1, 2008; 19(2): 553 - 562.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
K. S. McDonald
Regulation of cardiac muscle contraction: how paramount are the sarcomeres?
Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2007; 293(3): R961 - R962.
[Full Text] [PDF]

Home page
 J. Physiol.Home page
R. J. Solaro
Nitroxyl effects on myocardium provide new insights into the significance of altered myofilament response to calcium in the regulation of contractility
J. Physiol., May 1, 2007; 580(3): 697 - 697.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2007 by the Int. Union Physiol. Sci./Am. Physiol. Soc.