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Sodium-hydrogen exchange and its role in controlling contractility during acidosis in cardiac muscle

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Abstract

Intracellular pH (pHi) and Na (ana i) were recorded in isolated sheep cardiac Purkinje fibres using ion-selective microelectrodes while simultaneously recording twitch tension. A fall of (pHi) stimulated acid-extrusion via sarcolemmal Na-H exchange but the extrusion was inhibited by reducing extracellular pH (pHo), indicating an inhibitory effect of external H ions upon the exchanger. Intracellular acidosis can reduce contraction by directly reducing myofibrillar Ca2− sensitivity. The activation of Na-H exchange at low (pHi) can offset this direct inhibitory effect of H− ions since exchange-activation elevates ana i which then indirectly elevates Cai 2+ (via Na-Ca exchange) thus tending to restore tension. This protection of contraction during intracellular acidosis can be removed if extracellular (pHi) is also allowed to fall since, under these conditions, Na-H exchange is inhibited.

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Author notes

  1. C. Bountral

    Present address: Glaxo Group Research, Greenford, Middlesex, UK

Authors and Affiliations

  1. University Laboratory of Physiology, Parks Road, OX1 3PT, Oxford, UK

    R. D. Vaughan-Jones, Mei-Lin Wu & C. Bountral

Authors
  1. R. D. Vaughan-Jones
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  2. Mei-Lin Wu
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  3. C. Bountral
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Vaughan-Jones, R.D., Wu, ML. & Bountral, C. Sodium-hydrogen exchange and its role in controlling contractility during acidosis in cardiac muscle. Mol Cell Biochem 89, 157–162 (1989). https://doi.org/10.1007/BF00220769

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  • DOI: https://doi.org/10.1007/BF00220769

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