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Cardiovascular Research 1997 34(1):48-54; doi:10.1016/S0008-6363(97)00044-8
© 1997 by European Society of Cardiology
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Copyright © 1997, European Society of Cardiology

The regulation of intracellular pH in the diabetic myocardium

Danielle Feuvray*

Laboratoire de Physiologie Cellulaire, Université Paris XI, Bât. 443, 91405 Orsay Cedex, France

* Tel.: +33 (1) 69 15 78 98; fax: +33 (1) 69 15 68 41.

Received 25 October 1996; accepted 13 January 1997

KEYWORDS pHi regulation; Diabetes; Na+/H+ exchange; Na+- and HCO3–-dependent alkalinising transporter; Lactate–H+ co-transport

The first 150 words of the full text of this article appear below.

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   1 Introduction
 
In myocardial cells, as in any given cell, steady-state intracellular pH (pHi) is strictly maintained within a narrow range at relatively alkaline values. Resting pHi (7.1–7.2) is determined by the algebraic sum of acid-loading and acid-extruding processes. Whenever acid-loading exceeds acid extrusion, pHi falls. The degree to which pHi changes is inversely related to the intracellular buffering power (βi). The role of intracellular buffering power, which is the first line of defence of a cardiac cell against an intracellular acid–base disturbance, is to moderate pHi changes produced by acute acid (or alkali) load [1]. However, buffering mechanisms cannot prevent a change in pHi, but only reduce its amplitude. The regulation of pHi then largely depends upon the activity of plasma membrane carrier-mediated transport of acid/base equivalents [2, 3]. Intracellular pH is important for the activity of a number of enzymes with optimal pH within . . . [Full Text of this Article]


   2 pHi regulation in multicellular and single cell preparations
 

   3 pHi regulation in isolated hearts
 

   4 Concluding remarks
 

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