Jackson M J, Norris S H
J Physiol. 1985 Mar;360:293-310. doi: 10.1113/jphysiol.1985.sp015618.
The effects of ion substitution, inhibitors and variations in transmural p.d. on the movements of sodium and chloride across an in vitro preparation of rat gastric mucosa have been studied. The tissue maintained net steady-state transport of sodium in the mucosal-to-serosal direction in the absence of transmural gradients of electrochemical potential. Sodium transport was independent of the presence of chloride, and was abolished by 1 X 10(-5) M-amiloride. The inhibitor produced a decrease in short-circuit current equivalent to the depression of sodium transport, indicating that the sodium transport process was electrogenic. Variations in transmural p.d. showed that the sodium transport process included two components: one that varied with p.d. and one that was independent of it. These findings have been interpreted in terms of a system for sodium transport composed of three components: two rate-limiting entry mechanisms at the apical membrane, one of which can be represented as a conductive channel for sodium diffusion and the other as a neutral process possibly a sodium-hydrogen exchanger, and a voltage-independent pump at the basolateral membrane analogous to the constant-current pump models described in some other epithelia. The tissue maintained a net secretory movement of chloride in the short-circuited condition. The process responsible for net transport of chloride could be resolved into two components: one that was sodium dependent, electrogenic, and abolished by 8 X 10(-3) M-acetazolamide, and one that was independent of the presence of sodium, electrically silent and abolished by 5 X 10(-4) M-SITS (4-acetamido-4'-isothiocyano-2,2'-disulphonic acid stilbene). Both components of the chloride transport process varied with p.d. These findings were interpreted in terms of a system of three components: two entry mechanisms at the basolateral membrane including a coupled sodium-chloride influx process and a chloride-bicarbonate exchanger in parallel, and a rate-limiting conductive channel at the apical membrane. In addition, the studies on the effects of variations in transmural p.d. on chloride fluxes revealed a symmetrical voltage-independent component, dependent on the presence of chloride in the trans compartment, and it was suggested that this component may reflect the presence of a chloride-chloride exchange mechanism.
研究了离子替代、抑制剂以及跨膜电位变化对大鼠胃黏膜体外标本中钠和氯转运的影响。在不存在电化学势跨膜梯度的情况下，该组织维持了钠从黏膜到浆膜方向的净稳态转运。钠的转运不依赖于氯的存在，且被1×10⁻⁵ M的氨氯吡脒所阻断。该抑制剂使短路电流降低，降低程度与钠转运的抑制程度相当，表明钠转运过程是生电的。跨膜电位的变化表明，钠转运过程包括两个部分：一个随电位变化，另一个与之无关。这些发现可解释为钠转运系统由三个部分组成：顶端膜上的两个限速进入机制，其中一个可表示为钠扩散的传导通道，另一个为中性过程，可能是钠 - 氢交换体；以及基底外侧膜上与其他一些上皮中描述的恒流泵模型类似的电压不依赖泵。在短路状态下，该组织维持了氯的净分泌转运。负责氯净转运的过程可分为两个部分：一个依赖于钠，生电，且被8×10⁻³ M的乙酰唑胺所阻断；另一个与钠的存在无关，电沉默，且被5×10⁻⁴ M的SITS（4 - 乙酰氨基 - 4'-异硫氰基 - 2,2'-二磺酸芪）所阻断。氯转运过程的两个部分均随电位变化。这些发现可解释为一个由三个部分组成的系统：基底外侧膜上的两个进入机制，包括一个耦联的钠 - 氯内流过程和一个并行的氯 - 碳酸氢根交换体；以及顶端膜上的一个限速传导通道。此外，关于跨膜电位变化对氯通量影响的研究揭示了一个对称的电压不依赖成分，它依赖于跨膜隔室中氯的存在，有人认为该成分可能反映了氯 - 氯交换机制的存在。
