Binder H J, Murer H
J Membr Biol. 1986;91(1):77-84. doi: 10.1007/BF01870217.
These experiments were designed to determine whether proton-driven 86Rb uptake was present in apical membrane vesicles prepared from rat ileum. The uptake of 86Rb was approximately 300 to 350% greater in the presence of a 100-fold H+ gradient than in its absence and was greater at 1, 2 and 5 minutes ("overshoot") than that at 90 minutes. Proton-driven 86Rb uptake was decreased by 20% in TMA-nitrate compared to that in TMA-gluconate. 0.3 mM amiloride did not significantly inhibit proton-driven 86Rb uptake; in contrast, proton-driven 22Na uptake was significantly inhibited by 0.3 mM amiloride by 34%. Similarly, 25 mM KCl inhibited proton-driven 86Rb uptake more than that of 22Na, while the inhibition of proton-driven 22Na uptake by 25 mM NaCl was greater than that of 86Rb. In additional studies intravesicular acidification measured by acridine orange fluorescence was demonstrated in the presence of an outwardly directed K gradient. These studies demonstrate that a proton gradient stimulates 86Rb uptake and a K gradient induces intravesicular acidification; and that these fluxes are mediated by a K/H exchange distinct from Na/H exchange which is also present in this membrane. We conclude that a specific exchange process for K/H is located in ileal apical membrane vesicles.
这些实验旨在确定从大鼠回肠制备的顶端膜囊泡中是否存在质子驱动的⁸⁶Rb摄取。在存在100倍H⁺梯度的情况下，⁸⁶Rb的摄取比不存在时大约高300%至350%，并且在1、2和5分钟时（“过冲”）比90分钟时更高。与在TMA-葡萄糖酸盐中相比，在TMA-硝酸盐中质子驱动的⁸⁶Rb摄取减少了20%。0.3 mM氨氯地平并未显著抑制质子驱动的⁸⁶Rb摄取；相反，0.3 mM氨氯地平使质子驱动的²²Na摄取显著抑制了34%。同样，25 mM KCl对质子驱动的⁸⁶Rb摄取的抑制作用大于对²²Na摄取的抑制作用，而25 mM NaCl对质子驱动的²²Na摄取的抑制作用大于对⁸⁶Rb摄取的抑制作用。在另外的研究中，在存在外向K⁺梯度的情况下，通过吖啶橙荧光测量的囊泡内酸化得到了证实。这些研究表明质子梯度刺激⁸⁶Rb摄取，K⁺梯度诱导囊泡内酸化；并且这些通量是由与该膜中也存在的Na⁺/H⁺交换不同的K⁺/H⁺交换介导的。我们得出结论，K⁺/H⁺的特定交换过程位于回肠顶端膜囊泡中。
