Na+/H+ Exchange In Cardiac Cells: Implications For Electrical And Mechanical Events During Intracellular pH Changes
Intracellular acidification induced by changing from Hepes to a CO2/HCO− 3 buffer results in an increase in the intracellular Na+ activity (ai Na). The exchanger is nearly inactive at intracellular pH (pHi) of 7.2 − 7.0 and is strongly activated at pHi below 7.0. The rate of rise in ai Na in conditions of a blocked Na+/K+ pump increases by a factor of 3.8 ± 0.9 (n=6) when pHi drops from 7.2 ± 0.1 in Hepes to 6.8 ± 0.1 in 15% CO2. Acid-induced increase in ai Na and accelerated rate of rise of ai Na can be blocked by amiloride (2.10−3 M) or by decreasing pHO to 6.7. The rise in ai Na is associated with the generation of a Na+/K+ pump-dependent outward current. At low pHO the increase in outward current is much smaller which demonstrates the absence of secondary pump stimulation when Na+/H+ exchange is inhibited. The Na+/K+ pump dependent hyperpolarization modifies spontaneous activity. Recovery of contractile force in an acid-loaded cell is related to the gain in ai Na.
KeywordsIschemia Boron Bicarbonate Hepes Cardiol
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- Mahnensmith RL, Aronson PS (1985) The plasma membrane sodium-hydrogen exchanger and its role in physiological and pathophysiological processes. Circ Res 57: 773–788 )Google Scholar
- Verdonck F, Glitsch HG, Pusch H (1982) Importance of electrogenic sodium extrusion for suppression of spontaneous activity in rabbit Purkinje fibres. Arch int Physiol Biochim 90: 36–37Google Scholar