Regulation of intracellular pH in sheep cardiac Purkinje fibre: interactions among Na+, H+ and Ca2+
Kaila K., Vaughan-Jones RD., Bountra C.
Experiments were performed on sheep cardiac Purkinje fibres using pH- and sodium-selective microelectrodes, while simultaneously measuring tension, to determine if the fall in intracellular pH (pHi) following a rise in intracellular Na+ activity [Formula: see text] is caused by inhibition or reversal of acid extrusion on Na+–H+ exhange. A rise in [Formula: see text] was induced either by using the cardioactive steroid strophanthidin to inhibit the sarcolemmal Na+–K+ pump or by increasing the frequency of stimulation (0–4 Hz). Both of these manoeuvres led to an increase in [Formula: see text] and a decrease in pHi. Following exposure to strophanthidin, amiloride (an inhibitor of sarcolemmal Na+–H+ exchange) produced a decrease in both pHi and [Formula: see text]. These effects of amiloride increased with decreasing pHi, indicating that acid extrusion on Na+–H+ exchange is stimulated by the fall in pHi. The changes in intracellular Na+ and H+ caused by amiloride were quantitatively consistent with an electroneutral stoichiometry. The fall in pHi during strophanthidin exposure is therefore not caused by inhibition or reversal of acid extrusion Na+–H+ exchange. It is likely that the fall in pHi during a rate increase is also independent of Na+–H+ exchange. This is because (i) it has been shown previously to occur in the presence of amiloride and (ii) the calcium antagonist D600 completely abolished the stimulation-dependent fall in pHi. It is concluded that the intracellular acidosis following inhibition of the sarcolemmal Na+–K+ pump or following an increase in the rate of stimulation is secondary to a rise in intracellular calcium.