Halevy J, Budinger M E, Hayslett J P, Binder H J
Gastroenterology. 1986 Nov;91(5):1227-33. doi: 10.1016/s0016-5085(86)80021-x.
Dietary sodium depletion with elevated aldosterone levels induces electrogenic, amiloride-sensitive sodium absorption and inhibits electroneutral sodium chloride absorption in the rat distal colon. To assess the role of aldosterone in the production of these changes, unidirectional 22Na and 36Cl fluxes were performed under voltage clamp conditions across isolated distal colonic mucosa of rats given continuous aldosterone infusions for up to 12 days. Aldosterone infusion for 7-12 days produced identical changes in both electrogenic sodium absorption and electroneutral sodium chloride absorption compared with dietary sodium-depleted animals. In contrast, aldosterone at 24, 48, and 72 h produced varying changes in ion transport: electrogenic sodium absorption progressively increased, whereas electroneutral sodium chloride absorption was initially augmented but then inhibited. Aldosterone induced active potassium secretion, demonstrated by a reversed short-circuit current after addition of amiloride, in all experimental groups. These results demonstrate that the changes in ion transport observed in sodium-depleted animals are produced by aldosterone, and that aldosterone not only stimulates electrogenic sodium absorption and potassium secretion but in a time-dependent manner both stimulates and inhibits electroneutral sodium chloride absorption.
饮食中钠缺乏且醛固酮水平升高会诱导大鼠远端结肠产生电生性、对氨氯吡脒敏感的钠吸收,并抑制电中性氯化钠吸收。为评估醛固酮在这些变化产生过程中的作用,在电压钳制条件下,对连续输注醛固酮长达12天的大鼠分离的远端结肠黏膜进行单向22Na和36Cl通量测定。与饮食中钠缺乏的动物相比,输注醛固酮7至12天在电生性钠吸收和电中性氯化钠吸收方面产生了相同的变化。相反,在24、48和72小时时,醛固酮对离子转运产生了不同的变化:电生性钠吸收逐渐增加,而电中性氯化钠吸收最初增强但随后受到抑制。在所有实验组中,醛固酮诱导了活性钾分泌,这通过添加氨氯吡脒后短路电流的逆转得以证明。这些结果表明,在钠缺乏动物中观察到的离子转运变化是由醛固酮产生的,并且醛固酮不仅刺激电生性钠吸收和钾分泌,还以时间依赖性方式既刺激又抑制电中性氯化钠吸收。