| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
-adrenergic stimulation does not activate Na+-Ca2+ exchange current in guinea-pig, mouse and rat ventricular myocytes
1 Department of Cardiovascular Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan
2 Department of Physiology and Biophysics, Graduate School of Medicine, Kyoto University, Kyoto, Japan
* To whom correspondence should be addressed. E-mail: matsuoka{at}card.med.kyoto-u.ac.jp.
The effect of 
-adrenergic stimulation on cardiac Na+-Ca2+ exchange has been controversial. To clarify the effect, we measured Na+-Ca2+ exchange current (INCX) in voltage-clamped guinea-pig, mouse and rat ventricular cells. When INCX was defined as a 5 mM Ni2+-sensitive current in guinea-pig ventricular myocytes, 1 µM isoproterenol apparently augmented INCX by about 32%. However, this increase was due probably to contamination of the cAMP-dependent Cl- current (CFTR-Cl- current, ICFTR_Cl), because Ni2+ inhibited the activation of ICFTR_Cl by 1 µM isoproterenol, with a half-maximum concentration of 0.5 mM under the conditions where INCX was suppressed. 5 or 10 mM Ni2+ did not inhibit ICFTR_Cl activated by 10 µM forskolin, an activator of adenylate cyclase, suggesting that Ni2+ acted upstream of adenylate cyclase in the -adrenergic signaling pathway. Furthermore, in a low extracellular Cl- bath solution, 1 µM isoproterenol did not significantly alter the amplitude of Ni2+-sensitive INCX at +50 mV, which is close to the reversal potential of ICFTR_Cl. No change in INCX amplitude was induced by 10 µM forskolin. When INCX was activated by extracellular Ca2+, it was not significantly affected by 1 µM isoproterenol in guinea-pig, mouse or rat ventricular cells. We concluded that -adrenergic stimulation does not have significant effects on INCX in guinea-pig, mouse or rat ventricular myocytes.
This article has been cited by other articles:
|
|
 |
|
  S. Despa, A. L. Tucker, and D. M. Bers Phospholemman-Mediated Activation of Na/K-ATPase Limits [Na]i and Inotropic State During {beta}-Adrenergic Stimulation in Mouse Ventricular Myocytes Circulation, April 8, 2008; 117(14): 1849 - 1855. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Kim and S. Matsuoka Cytoplasmic Na+-dependent modulation of mitochondrial Ca2+ via electrogenic mitochondrial Na+-Ca2+ exchange J. Physiol., March 15, 2008; 586(6): 1683 - 1697. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. N. Ebert and D. G. Taylor Catecholamines and development of cardiac pacemaking: An intrinsically intimate relationship Cardiovasc Res, December 1, 2006; 72(3): 364 - 374. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Takeuchi, S. Tatsumi, N. Sarai, K. Terashima, S. Matsuoka, and A. Noma Ionic Mechanisms of Cardiac Cell Swelling Induced by Blocking Na+/K+ Pump As Revealed by Experiments and Simulation J. Gen. Physiol., November 1, 2006; 128(5): 495 - 507. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. C. P. Haigney, S.-k. Wei, D. H. Schulze, A. M. Ruknudin, and S. Matsuoka Response to "beta-adrenergic stimulation does not activate Na+/Ca2+ exchange current in guinea pig, mouse, and rat ventricular myocytes" Am J Physiol Cell Physiol, April 1, 2006; 290(4): C1271 - C1271. [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
