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Cardiovascular Research 2001 52(3):339-344; doi:10.1016/S0008-6363(01)00497-7
© 2001 by European Society of Cardiology
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Copyright © 2001, European Society of Cardiology

Unmasking of a novel target for blocking harmful Na+ coupled acid extrusion: electrogenic Na+–HCO3 symport

Jos M.J Lamers*

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
 
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 . . . [Full Text of this Article]


    2. Molecular identity, modulation and expression of myocardial H+ transporters
 

    3. Implications of the alterations in expression of myocardial H+ transporters
 

    4. Myocardial ischemia and reperfusion and harmful Na+-coupled acid extrusion
 

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