© 2001 by European Society of Cardiology
Copyright © 2001, European Society of Cardiology
Unmasking of a novel target for blocking harmful Na+ coupled acid extrusion: electrogenic Na+–HCO3– symport
Department of Biochemistry, Cardiovascular Research Institute COEUR, Faculty of Medicine and Health Sciences, Erasmus University, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands
* Tel.: +31-10-408-7335; fax: +31-10-408-9472 lamers@bc1.fgg.eur.nl
accepted 4 October 2001
KEYWORDS Ischemia; Reperfusion; Ion exchangers; Na/H-exchanger; Heart failure; Acidosis
| The first 150 words of the full text of this article appear below. |
See article by Kandoudi et al. [22] (pages 388–396 in this issue).
| 1. Regulation of myocardial pHi |
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Many cellular functions of myocardium, such as the sensitivity of the myofilaments to Ca2+, the activity of the rate-limiting enzyme of the glycolysis (1-phosphofructokinase) and number of functional gap junctions between adjacent myocytes, are strongly affected by lowering of pHi [1]. In fact, acidosis depresses contractility in cardiac myocytes by affecting virtually every step in the excitation–contraction coupling [2]. On the other hand, there is also evidence that cytoplasmic alkalinization is an intracellular messenger mediating growth responses of various stimuli such as stretch, neurohumoral factors and growth factors [3]. Therefore, in order to preserve proper cardiac functioning, pHi of the myocytes is maintained within narrow limits. Normally myocardial pHi is about one pH unit more alkaline than would be expected if H+ was in electrochemical equilibrium [4–7]. This indicates the existence of mechanisms
| 2. Molecular identity, modulation and expression of myocardial H+ transporters |
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| 3. Implications of the alterations in expression of myocardial H+ transporters |
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| 4. Myocardial ischemia and reperfusion and harmful Na+-coupled acid extrusion |
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