Chen J S, Walser M
J Membr Biol. 1975 Apr 23;21(1-2):87-98. doi: 10.1007/BF01941063.
To assess the active components of sodium flux across toad bladder as a function of transepithelial potential, unidirectional sodium fluxes between identical media were measured before and after adding sufficient ouabain (1.89 X 10(-3)M) to eliminate active transport, while clamping transepithelial potential to 0, 100 or 150 mV. Evidence was adduced that ouabain does not alter passive fluxes, and that fluxes remain constant if ouabain is not added. Hence, the ouabain-inhibitable fluxes represent fluxes through the active path. Results were analyzed by a set of equations, previously shown to describe adequately passive fluxes under electrical gradients in this tissue, here modified by the insertion of E, the potential at which bidirectional sodium fluxes (beta E, and theta E) through the active pathway are equal. According to these equations, beta E and theta E are the logarithmic mean of bidirectional fluxes through the active path at any potential, and the flux ratio in this path is modified by a constant factor Qia, which represents the ratio of the bulk diffusion coefficient to the tracer diffusion coefficient in this pathway. The data are shown to conform closely to these equations. Qia averages 2.54. Hence, serosal-to-mucosal flux vanishes rapidly as potential falls below E. Mean E in these experiments was 158 +/- 1 mV. Thus, linear dependence of net flux in both active and passive pathways on potential is present, even though the sodium fluxes in both paths fail to conform to the Ussing flux ratio equation. Qip less than 1 in the passive path (qualitatively similar to exchange diffusion) and Qia greater than 1 in the active path (as in single file pore diffusion). Both of these features tend to reduce the change in serosal-to-mucosal sodium flux induced by depolarization from spontaneous potential to zero potential ("short-circuiting").
为了评估蟾蜍膀胱跨上皮钠通量的活性成分与跨上皮电位的关系，在添加足量哇巴因（1.89×10⁻³M）以消除主动转运前后，测量相同介质之间的单向钠通量，同时将跨上皮电位钳制在0、100或150 mV。有证据表明哇巴因不会改变被动通量，且不添加哇巴因时通量保持恒定。因此，哇巴因可抑制的通量代表通过活性途径的通量。结果通过一组方程进行分析，这些方程先前已被证明能充分描述该组织在电场梯度下的被动通量，此处通过插入E进行了修正，E是通过活性途径的双向钠通量（βE和θE）相等时的电位。根据这些方程，βE和θE是在任何电位下通过活性途径的双向通量的对数平均值，且该途径中的通量比由常数因子Qia修正，Qia代表该途径中本体扩散系数与示踪剂扩散系数的比值。数据显示与这些方程非常吻合。Qia的平均值为2.54。因此，当电位降至E以下时，浆膜到黏膜的通量迅速消失。这些实验中的平均E为158±1 mV。因此，即使两条途径中的钠通量不符合乌斯辛通量比方程，活性和被动途径中的净通量对电位仍存在线性依赖性。被动途径中的Qip小于1（定性上类似于交换扩散），活性途径中的Qia大于1（如在单通道孔扩散中）。这两个特征都倾向于减少从自发电位去极化到零电位（“短路”）所引起的浆膜到黏膜钠通量的变化。
