Sodium-hydrogen exchange and its role in controlling contractility during acidosis in cardiac muscle.
Intracellular pH (pHi) and Na (aina) 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 aina which then indirectly elevates Ca2+i (via Na-Ca exchange) thus tending to restore tension. This protection of contraction during intracellular acidosis can be removed if extracellular pH is also allowed to fall since, under these conditions, Na-H exchange is inhibited.
Vaughan-Jones
R D
RD
University Laboratory of Physiology, Oxford, UK.
Wu
M L
ML
Bountra
C
C
D000138:Acidosis / Q000378:metabolism*; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002352:Carrier Proteins / Q000378:metabolism*; D006863:Hydrogen-Ion Concentration; D007474:Ion Exchange; D008564:Membrane Potentials; D009200:Myocardial Contraction / Q000502:physiology*; D009206:Myocardium / Q000378:metabolism*; D011690:Purkinje Fibers / Q000378:metabolism; D012756:Sheep; D012964:Sodium / Q000378:metabolism*; D017923:Sodium-Hydrogen Exchangers
D002352:Carrier Proteins; D017923:Sodium-Hydrogen Exchangers; D012964:Sodium; D002118:Calcium