Kaila K, Vaughan-Jones R D, Bountra C
Can J Physiol Pharmacol. 1987 May;65(5):963-9. doi: 10.1139/y87-153.
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 (aiNa) is caused by inhibition or reversal of acid extrusion on Na+-H+ exchange. A rise in aiNa 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 aiNa and a decrease in pHi. Following exposure to strophanthidin, amiloride (an inhibitor of sarcolemmal Na+-H+ exchange) produced a decrease in both pHi and aiNa. 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.
利用pH和钠选择性微电极对绵羊心脏浦肯野纤维进行实验，同时测量张力，以确定细胞内Na⁺活性（aiNa）升高后细胞内pH（pHi）下降是否由Na⁺-H⁺交换的酸排出抑制或逆转引起。通过使用强心甾体毒毛花苷抑制肌膜Na⁺-K⁺泵或增加刺激频率（0 - 4Hz）来诱导aiNa升高。这两种操作均导致aiNa升高和pHi下降。暴露于毒毛花苷后，氨氯地平（肌膜Na⁺-H⁺交换抑制剂）使pHi和aiNa均降低。氨氯地平的这些作用随pHi降低而增强，表明pHi下降刺激了Na⁺-H⁺交换的酸排出。氨氯地平引起的细胞内Na⁺和H⁺变化在数量上与电中性化学计量一致。因此，毒毛花苷暴露期间pHi下降并非由酸排出Na⁺-H⁺交换的抑制或逆转引起。心率增加期间pHi下降可能也与Na⁺-H⁺交换无关。这是因为（i）先前已证明在氨氯地平存在时会发生这种情况，以及（ii）钙拮抗剂D600完全消除了刺激依赖性pHi下降。得出的结论是，肌膜Na⁺-K⁺泵抑制后或刺激速率增加后发生的细胞内酸中毒继发于细胞内钙升高。
