Arruda J A, Dytko G, Mola R, Kurtzman N A
Kidney Int. 1980 Feb;17(2):196-204. doi: 10.1038/ki.1980.23.
The mechanism whereby lithium impairs urinary acidification was investigated in vitro with the bladder of the fresh water turtle. The effect of lithium was compared to that of choline or cesium. In the presence of 1% carbon dioxide, lithium (40 mM in the mucosa) failed to alter hydrogen ion secretion. Lithium also caused a significant decrease in sodium transport and in potential difference. Lithium failed to increase the passive loss of hydrogen ions from the mucosal solution, indicating that it does not affect the permeability of the mucosa to hydrogen ions. Bicarbonate secretion also was unchanged in lithium-treated hemibladders. Under open-circuit conditions, lithium caused a significant decrease in potential difference and, hence, caused a significant decrease in hydrogen ion secretion. Restoration of the potential difference, in the presence of lithium, to control levels caused a return of hydrogen ion secretion to the original value. These data demonstrate that in the turtle baldder lithium inhibits hydrogen ion secretion solely by reducing the potential difference and suggest that in vivo lithium causes an acidification defect not by directly inhibiting the hydrogen ion pump or causing a hydrogen ion backleak but by inhibiting sodium transport, thereby decreasing the favorable electric gradient for hydrogen ion secretion.
利用淡水龟的膀胱在体外研究了锂损害尿液酸化的机制。将锂的作用与胆碱或铯的作用进行了比较。在存在1%二氧化碳的情况下，锂（黏膜中浓度为40 mM）未能改变氢离子分泌。锂还导致钠转运和电位差显著降低。锂未能增加黏膜溶液中氢离子的被动损失，表明它不影响黏膜对氢离子的通透性。在锂处理的半膀胱中，碳酸氢盐分泌也未改变。在开路条件下，锂导致电位差显著降低，因此导致氢离子分泌显著减少。在存在锂的情况下将电位差恢复到对照水平会使氢离子分泌恢复到原始值。这些数据表明，在龟膀胱中锂仅通过降低电位差来抑制氢离子分泌，并表明在体内锂导致酸化缺陷不是通过直接抑制氢离子泵或导致氢离子回漏，而是通过抑制钠转运，从而降低氢离子分泌的有利电梯度。
