Ziegler T W, Fanestil D D, Ludens J H
Kidney Int. 1976 Oct;10(4):279-86. doi: 10.1038/ki.1976.110.
The rate of urinary acidification by toad urinary bladders was measured in vitro by following the pH changes of the HCO3-/CO2-buffered Ringer's solutions bathing the mucosal and serosal sides of the bladder. Within the tolerated range of transepithelial potential differences (PD) (-100 to +100 mv), the rate of acidification was found to be a linear function of the PD. The rate of acidification could be increased by a favorable PD whether the PD was the spontaneous transepithelial PD due to sodium transport or a PD imposed in the absence of sodium transport, as when choline was substituted for Na or when amiloride blocked sodium transport. Acetazolamide inhibited both active and PD-driven acidification. Acidification rate was the same in 2.4 mM HCO3- and 1% CO2 as in 12 mM HCO3- and 5% CO2; again, acidification was increased equally by a favorable PD. PD-driven acidification was found to be linearly correlated with acidification occurring at short-circuit conditions. These findings suggest that the rate of acidification can be accelerated by the transepithelial PD in the absence of sodium transport and that the PD-driven component of acidification utilizes a transcellular pathway.
通过跟踪蟾蜍膀胱黏膜和浆膜侧HCO3-/CO2缓冲林格氏液的pH变化,体外测量蟾蜍膀胱的尿酸化速率。在跨上皮电位差(PD)的耐受范围内(-100至+100 mV),发现酸化速率是PD的线性函数。无论PD是由于钠转运引起的自发跨上皮PD,还是在无钠转运时施加的PD,如用胆碱替代Na或用氨氯吡咪阻断钠转运时,有利的PD均可提高酸化速率。乙酰唑胺抑制主动酸化和PD驱动的酸化。2.4 mM HCO3-和1% CO2条件下的酸化速率与12 mM HCO3-和5% CO2条件下相同;同样,有利的PD同样会增加酸化。发现PD驱动的酸化与短路条件下发生的酸化呈线性相关。这些发现表明,在无钠转运时,跨上皮PD可加速酸化速率,且PD驱动的酸化成分利用了跨细胞途径。