Skip Navigation

Cardiovascular Research 1999 44(2):398-406; doi:10.1016/S0008-6363(99)00205-9
© 1999 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Kinugawa, S.
Right arrow Articles by Takeshita, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kinugawa, S.
Right arrow Articles by Takeshita, A.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 1999, European Society of Cardiology

Role of Ca2+ availability to myofilaments and their sensitivity to Ca2+ in myocyte contractile dysfunction in heart failure

Shintaro Kinugawa, Hiroyuki Tsutsui*, Shinji Satoh, Masaru Takahashi, Tomomi Ide, Keiko Igarashi-Saito, Ken-ichi Arimura, Kensuke Egashira and Akira Takeshita

Research Institute of Angiocardiology and Cardiovascular Clinic, Kyushu University School of Medicine, Fukuoka 812-8582, Japan

* Corresponding author. Tel.: +81-92-642-5360; fax: +81-92-642-5374 prehiro{at}cardiol.med.kyushu-u.ac.jp

Objective: Contractile function is depressed at the isolated myocyte level in heart failure (HF), which could result from the decreased availability of intracellular calcium ([Ca2+]i) to the myofibrils and/or the depressed sensitivity of myofilaments to [Ca2+]i. However, the cellular basis of contractile dysfunction remains unestablished. Methods: We isolated left ventricular myocytes from dogs with rapid pacing-induced HF. Cell shortening and [Ca2+]i transients were measured by indo-1 fluorescence and the myofilament Ca2+ sensitivity was analyzed by the shortening–[Ca2+]i relation in intact myocytes as well as by the pCa–tension relation in skinned cells. Results: Peak cell shortening magnitude was depressed in HF, associated with a parallel decrease of [Ca2+]i transient amplitude. There was a significant positive correlation between these two variables (r=0.71, P<0.01). In contrast, myofibrillar sensitivity to Ca2+, determined by both intact and skinned myocytes, was comparable between control and HF. Further, there was no significant difference in Ca2+ sensitivity between control and HF even at shorter (1.8 µm) or longer (2.2 µm) sarcomere length. Conclusions: Using both intact and skinned cellular preparations, a potential defect in myocyte contractile function in HF was a reduction in Ca2+ availability to the myofilaments, rather than the inherent defects in myofilament sensitivity to Ca2+.

KEYWORDS Calcium (cellular); Cell culture/isolation; Contractile function; Heart failure; Myocytes


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Circ Heart FailHome page
K. D. Varian, A. Kijtawornrat, S. C. Gupta, C. A.A. Torres, M. M. Monasky, N. Hiranandani, D. A. Delfin, J. A. Rafael-Fortney, M. Periasamy, R. L. Hamlin, et al.
Impairment of Diastolic Function by Lack of Frequency-Dependent Myofilament Desensitizationin Rabbit Right Ventricular Hypertrophy
Circ Heart Fail, September 1, 2009; 2(5): 472 - 481.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
N. S. Dhalla, H. K. Saini-Chohan, D. Rodriguez-Leyva, V. Elimban, M. R. Dent, and P. S. Tappia
Subcellular remodelling may induce cardiac dysfunction in congestive heart failure
Cardiovasc Res, February 15, 2009; 81(3): 429 - 438.
[Abstract] [Full Text] [PDF]


Home page
J. Physiol.Home page
I. Sjaastad, J A. Wasserstrom, and O. M Sejersted
Heart failure - a challenge to our current concepts of excitation-contraction coupling
J. Physiol., January 1, 2003; 546(1): 33 - 47.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
H. Tsutsui, T. Ide, S. Hayashidani, N. Suematsu, H. Utsumi, R. Nakamura, K. Egashira, and A. Takeshita
Greater susceptibility of failing cardiac myocytes to oxygen free radical-mediated injury
Cardiovasc Res, January 1, 2001; 49(1): 103 - 109.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.