Pandiyan V, Rajendran V M, Binder H J
Department of Internal Medicine, Yale University, New Haven, Connecticut.
Gastroenterology. 1992 Jun;102(6):1846-53. doi: 10.1016/0016-5085(92)90304-h.
To determine the effect of mucosal sodium and mucosal ouabain on active Rb+(K+) absorption, unidirectional and net 86Rb+ fluxes were measured under voltage-clamp conditions in the distal colon of normal and sodium-depleted rats. The role of mucosal sodium (independent of serosal sodium) was evaluated in a model of Rb+(K+) absorption in which serosal ouabain markedly enhanced active Rb+(K+) absorption. In normal rats, mucosal sodium was a competitive inhibitor of Rb+(K+) absorption, and Rb+(K+) absorption consisted of a mucosal sodium-sensitive component and a mucosal sodium-insensitive component. Further, mucosal ouabain almost completely inhibited the mucosal sodium-insensitive component but did not affect the mucosal sodium-sensitive component. In sodium-depleted rats, both mucosal sodium-sensitive and mucosal sodium-insensitive fractions of Rb+(K+) absorption were also identified. Aldosterone markedly stimulated the mucosal sodium-sensitive component (1.68 +/- 0.15 vs. 0.60 +/- 0.10 muEq.h-1.cm-2) but not the sodium-insensitive component (0.88 +/- 0.09 vs. 0.64 +/- 0.06 muEq.h-1.cm-2) component of Rb+(K+) absorption; however, in contrast to normal animals, mucosal sodium in sodium-depleted animals was a noncompetitive inhibitor of Rb+(K+) absorption. The mucosal sodium-insensitive component of Rb+(K+) absorption in sodium-depleted animals was substantially inhibited by mucosal ouabain, but the mucosal sodium-sensitive component, unlike that in normal animals, was partially inhibited by mucosal ouabain. These studies indicate that the characteristics of the Rb+(K+) absorptive process in sodium-depleted animals differ significantly from those present in normal animals, suggesting that aldosterone induces an Rb+(K+) absorptive mechanism not present in normal animals.
为了确定黏膜钠和黏膜哇巴因对Rb⁺(K⁺)主动吸收的影响,在电压钳制条件下,测量了正常大鼠和缺钠大鼠远端结肠的单向和净⁸⁶Rb⁺通量。在Rb⁺(K⁺)吸收模型中评估了黏膜钠(独立于浆膜钠)的作用,在该模型中,浆膜哇巴因显著增强了Rb⁺(K⁺)的主动吸收。在正常大鼠中,黏膜钠是Rb⁺(K⁺)吸收的竞争性抑制剂,且Rb⁺(K⁺)吸收由黏膜钠敏感成分和黏膜钠不敏感成分组成。此外,黏膜哇巴因几乎完全抑制了黏膜钠不敏感成分,但不影响黏膜钠敏感成分。在缺钠大鼠中,也确定了Rb⁺(K⁺)吸收的黏膜钠敏感和黏膜钠不敏感部分。醛固酮显著刺激了Rb⁺(K⁺)吸收的黏膜钠敏感成分(1.68±0.15对0.60±0.10μEq·h⁻¹·cm⁻²),但不刺激钠不敏感成分(0.88±0.09对0.64±0.06μEq·h⁻¹·cm⁻²);然而,与正常动物不同,缺钠动物中的黏膜钠是Rb⁺(K⁺)吸收的非竞争性抑制剂。缺钠动物中Rb⁺(K⁺)吸收的黏膜钠不敏感成分被黏膜哇巴因显著抑制,但与正常动物不同,黏膜钠敏感成分被黏膜哇巴因部分抑制。这些研究表明,缺钠动物中Rb⁺(K⁺)吸收过程的特征与正常动物有显著差异,提示醛固酮诱导了正常动物中不存在的Rb⁺(K⁺)吸收机制。