Published online before print August 1, 2002, doi: 10.1161/01.RES.0000031384.55006.DB
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on April 4, 2002
Revised on July 15, 2002
Accepted on July 18, 2002
Increased Exchange Current but Normal Ca2+ Transport via Na+-Ca2+ Exchange During Cardiac Hypertrophy After Myocardial Infarction
Ana Maria Gómez ;
From the Departments of Physiology (E.N., M.E.) and Pharmacology (H.P.), University of Bern, Bern, Switzerland; INSERM U390 (A.M.G., G.V.), CHU A. de Villeneuve, Montpellier, France; and the University of Fribourg (B.S.), Department of Histology and General Embryology, Switzerland.
* To whom correspondence should be addressed. E-mail: egger{at}pyl.unibe.ch.
Hypertrophied and failing cardiac myocytes generally show alterations in intracellular Ca2+ handling associated with changes in the contractile function and arrhythmogenicity. The cardiac Na+-Ca2+ exchange (NCX) is an important mechanism for Ca2+ extrusion and cell relaxation. Its possible involvement in changes of excitation-contraction coupling (EC-coupling) with disease remains uncertain. We analyzed the NCX function in rat ventricular myocytes 5 to 6 months after experimental myocardial infarction (PMI) produced by left coronary artery ligation and from sham-operated (SO) hearts. Caged Ca2+ was dialyzed into the cytoplasm via a patch-clamp pipette and Ca2+ was released by flash photolysis to activate NCX and measure the associated currents (INaCa), whereas [Ca2+]i changes were simultaneously recorded with a confocal microscope. INaCa density normalized to the [Ca2+]i jumps was 2.6-fold higher in myocytes from PMI rats. The level of total NCX protein expression in PMI myocytes was also increased. Interestingly, although the INaCa density in PMI cells was larger, PMI and SO myocytes presented virtually identical Ca2+ transport via the NCX. This discrepancy was explained by a reduced surface/volume ratio (34.8%) observed in PMI cells. We conclude that the increase in NCX density may be a mechanism to maintain the required Ca2+ extrusion from a larger cell to allow adequate relaxation.
Key words: sodium--calcium exchange • cardiac myocyte • hypertrophy • intracellular calcium • calcium transport
This article has been cited by other articles:
 |
|
 |
|
  K. Gusev, A. A. Domenighetti, L. M.D. Delbridge, T. Pedrazzini, E. Niggli, and M. Egger Angiotensin II-Mediated Adaptive and Maladaptive Remodeling of Cardiomyocyte Excitation-Contraction Coupling Circ. Res., July 2, 2009; 105(1): 42 - 50. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Aharinejad, D. Abraham, P. Paulus, K. Zins, M. Hofmann, W. Michlits, M. Gyongyosi, K. Macfelda, T. Lucas, K. Trescher, et al. Colony-stimulating factor-1 transfection of myoblasts improves the repair of failing myocardium following autologous myoblast transplantation Cardiovasc Res, August 1, 2008; 79(3): 395 - 404. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. R. Heinzel, V. Bito, L. Biesmans, M. Wu, E. Detre, F. von Wegner, P. Claus, S. Dymarkowski, F. Maes, J. Bogaert, et al. Remodeling of T-Tubules and Reduced Synchrony of Ca2+ Release in Myocytes From Chronically Ischemic Myocardium Circ. Res., February 15, 2008; 102(3): 338 - 346. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. S. Dhalla, M. R. Dent, P. S. Tappia, R. Sethi, J. Barta, and R. K. Goyal Subcellular Remodeling as a Viable Target for the Treatment of Congestive Heart Failure Journal of Cardiovascular Pharmacology and Therapeutics, March 1, 2006; 11(1): 31 - 45. [Abstract] [PDF]
|
|
|
|
 |
|
 L. Pereira, J. Matthes, I. Schuster, H. H. Valdivia, S. Herzig, S. Richard, and A. M. Gomez Mechanisms of [Ca2+]i Transient Decrease in Cardiomyopathy of db/db Type 2 Diabetic Mice Diabetes, March 1, 2006; 55(3): 608 - 615. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Maeda, I. Matsuoka, T. Iwamoto, H. Kurose, and J. Kimura Down-Regulation of Na+/Ca2+ Exchanger by Fluvastatin in Rat Cardiomyoblast H9c2 Cells: Involvement of RhoB in Na+/Ca2+ Exchanger mRNA Stability Mol. Pharmacol., August 1, 2005; 68(2): 414 - 420. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. A. Domenighetti, Q. Wang, M. Egger, S. M. Richards, T. Pedrazzini, and L. M.D. Delbridge Angiotensin II-Mediated Phenotypic Cardiomyocyte Remodeling Leads to Age-Dependent Cardiac Dysfunction and Failure Hypertension, August 1, 2005; 46(2): 426 - 432. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Ouvrard-Pascaud, Y. Sainte-Marie, J.-P. Benitah, R. Perrier, C. Soukaseum, A. N. D. Cat, A. Royer, K. Le Quang, F. Charpentier, S. Demolombe, et al. Conditional Mineralocorticoid Receptor Expression in the Heart Leads to Life-Threatening Arrhythmias Circulation, June 14, 2005; 111(23): 3025 - 3033. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Q. Shao, B. Ren, V. Elimban, P. S. Tappia, N. Takeda, and N. S. Dhalla Modification of sarcolemmal Na+-K+-ATPase and Na+/Ca2+ exchanger expression in heart failure by blockade of renin-angiotensin system Am J Physiol Heart Circ Physiol, June 1, 2005; 288(6): H2637 - H2646. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. M. Gomez, I. Schuster, J. Fauconnier, J. Prestle, G. Hasenfuss, and S. Richard FKBP12.6 overexpression decreases Ca2+ spark amplitude but enhances [Ca2+]i transient in rat cardiac myocytes Am J Physiol Heart Circ Physiol, November 1, 2004; 287(5): H1987 - H1993. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Song, X.-Q. Zhang, J. Wang, L. L. Carl, B. A. Ahlers, L. I. Rothblum, and J. Y. Cheung Sprint training improves contractility in postinfarction rat myocytes: role of Na+/Ca2+ exchange J Appl Physiol, August 1, 2004; 97(2): 484 - 490. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. C. Lieber, N. Aubry, J. Pain, G. Diaz, S.-J. Kim, and S. F. Vatner Aging increases stiffness of cardiac myocytes measured by atomic force microscopy nanoindentation Am J Physiol Heart Circ Physiol, August 1, 2004; 287(2): H645 - H651. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M.E Diaz, H.K Graham, and A.W Trafford Enhanced sarcolemmal Ca2+ efflux reduces sarcoplasmic reticulum Ca2+ content and systolic Ca2+ in cardiac hypertrophy Cardiovasc Res, June 1, 2004; 62(3): 538 - 547. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
U. Kirchhefer, L. R Jones, F. Begrow, P. Boknik, L. Hein, M. J Lohse, B. Riemann, W. Schmitz, J. Stypmann, and J. Neumann Transgenic triadin 1 overexpression alters SR Ca2+ handling and leads to a blunted contractile response to {beta}-adrenergic agonists Cardiovasc Res, April 1, 2004; 62(1): 122 - 134. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. I. Spencer and J. S. K. Sham Effects of Na+/Ca2+ exchange induced by SR Ca2+ release on action potentials and afterdepolarizations in guinea pig ventricular myocytes Am J Physiol Heart Circ Physiol, December 1, 2003; 285(6): H2552 - H2562. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. W. Rodenbaugh, H. L. Collins, D. G. Nowacek, and S. E. DiCarlo Increased susceptibility to ventricular arrhythmias is associated with changes in Ca2+ regulatory proteins in paraplegic rats Am J Physiol Heart Circ Physiol, December 1, 2003; 285(6): H2605 - H2613. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F R Quinn, S Currie, A M Duncan, S Miller, R Sayeed, S M Cobbe, and G L Smith Myocardial infarction causes increased expression but decreased activity of the myocardial Na+--Ca2+ exchanger in the rabbit J. Physiol., November 15, 2003; 553(1): 229 - 242. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Brette and C. Orchard T-Tubule Function in Mammalian Cardiac Myocytes Circ. Res., June 13, 2003; 92(11): 1182 - 1192. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|