AJP - Heart Add DOIs to your references at manuscript stage!
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol 275: H1441-H1448, 1998;
0363-6135/98 $5.00
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 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 Google Scholar
Google Scholar
Right arrow Articles by Yao, A.
Right arrow Articles by Barry, W. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yao, A.
Right arrow Articles by Barry, W. H.
Vol. 275, Issue 4, H1441-H1448, October 1998

Abnormal myocyte Ca2+ homeostasis in rabbits with pacing-induced heart failure

Atsushi Yao1, Zhi Su1, Akihiko Nonaka1, Iram Zubair1, Kenneth W. Spitzer2, John H. B. Bridge2, Gerhard Muelheims1, John Ross Jr.3, and William H. Barry1

1 Division of Cardiology and 2 Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah Health Sciences Center, Salt Lake City, Utah 84132; and 3 Cardiology Division, University of California, San Diego, California 92093

To determine whether there are abnormalities in myocyte excitation-contraction coupling and intracellular Ca2+ concentration ([Ca2+]i) homeostasis in pacing-induced heart failure (PF), we measured L-type Ca2+ current (ICa,L) and Na+/Ca2+ exchanger current (INa/Ca) with voltage clamp and measured intracellular Na+ concentration ([Na+]i) and [Ca2+]i with the use of sodium-binding benzofuran isophthalate (SBFI) and fluo 3 in ventricular myocytes isolated from control and paced rabbits. The peak systolic and diastolic levels and the amplitude of electrically stimulated [Ca2+]i transients (0.25 Hz, extracellular Ca2+ concentration = 1.08 mM) were significantly less in PF myocytes. Also, there was prolongation of the times to peak and decline of [Ca2+]i transients. ICa,L density was markedly decreased in PF myocytes. INa/Ca at -40 mV elicited by rapid exposure to 0 Na+ solution with a rapid solution switcher was significantly reduced in PF myocytes, suggesting that the function of the Na+/Ca2+ exchanger is impaired in these myocytes. In PF myocytes the decline of the [Ca2+]i transient when the Na+/Ca2+ exchanger was abruptly disabled was markedly prolonged compared with the decline in control myocytes, consistent with depressed sarcoplasmic reticulum (SR) Ca2+-ATPase function. RNase protection assay showed decreased levels of Na+/Ca2+ exchanger and SR Ca2+-ATPase mRNA in PF hearts, consistent with the function studies. We conclude that the functions of L-type Ca2+ channels, Na+/Ca2+ exchanger, and SR Ca2+-ATPase are impaired in myocytes from rabbit hearts with failure induced by rapid pacing. These abnormalities result in reduced [Ca2+]i transients and systolic and diastolic dysfunction and appear to account for the abnormal ventricular function observed.

isolated myocyte; calcium transient; calcium channel; sodium/calcium exchanger; sarcoplasmic reticulum calcium adenosine 5'-triphosphatase


This article has been cited by other articles:


Home page
 Physiol. Rev.Home page
S. Nattel, A. Maguy, S. Le Bouter, and Y.-H. Yeh
Arrhythmogenic Ion-Channel Remodeling in the Heart: Heart Failure, Myocardial Infarction, and Atrial Fibrillation
Physiol Rev, April 1, 2007; 87(2): 425 - 456.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
G. Munch, K. Rosport, C. Baumgartner, Z. Li, S. Wagner, A. Bultmann, and M. Ungerer
Functional alterations after cardiac sodium-calcium exchanger overexpression in heart failure
Am J Physiol Heart Circ Physiol, August 1, 2006; 291(2): H488 - H495.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
C. L. Elias, A. Lukas, S. Shurraw, J. Scott, A. Omelchenko, G. J. Gross, M. Hnatowich, and L. V. Hryshko
Inhibition of Na+/Ca2+ exchange by KB-R7943: transport mode selectivity and antiarrhythmic consequences
Am J Physiol Heart Circ Physiol, September 1, 2001; 281(3): H1334 - H1345.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
S. M. Pogwizd
Increased Na+-Ca2+ Exchanger in the Failing Heart
Circ. Res., October 13, 2000; 87(8): 641 - 643.
[Full Text] [PDF]

Home page
 Circ. Res.Home page
I. A. Hobai and B. O'Rourke
Enhanced Ca2+-Activated Na+-Ca2+ Exchange Activity in Canine Pacing-Induced Heart Failure
Circ. Res., October 13, 2000; 87(8): 690 - 698.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
K. Ito, X. Yan, M. Tajima, Z. Su, W. H. Barry, and B. H. Lorell
Contractile Reserve and Intracellular Calcium Regulation in Mouse Myocytes From Normal and Hypertrophied Failing Hearts
Circ. Res., September 29, 2000; 87(7): 588 - 595.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
S. Nattel and D. Li
Ionic Remodeling in the Heart : Pathophysiological Significance and New Therapeutic Opportunities for Atrial Fibrillation
Circ. Res., September 15, 2000; 87(6): 440 - 447.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
S. M. Pogwizd, M. Qi, W. Yuan, A. M. Samarel, and D. M. Bers
Upregulation of Na+/Ca2+ Exchanger Expression and Function in an Arrhythmogenic Rabbit Model of Heart Failure
Circ. Res., November 26, 1999; 85(11): 1009 - 1019.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
L. Lu, D. F. Mei, A.-G. Gu, S. Wang, B. Lentzner, D. E. Gutstein, D. Zwas, S. Homma, G.-H. Yi, and J. Wang
Exercise training normalizes altered calcium-handling proteins during development of heart failure
J Appl Physiol, April 1, 2002; 92(4): 1524 - 1530.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online