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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