Lewis S A, Diamond J M
J Membr Biol. 1976 Aug 27;28(1):1-40. doi: 10.1007/BF01869689.
By in vitro experiments on rabbit bladder, we reassessed the traditional view that mammalian urinary bladder lacks ion transport mechanisms. Since the ratio of actual-to-nominal membrane area in folded epithelia is variable and hard to estimate, we normalized membrane properties to apical membrane capacitance rather than to nominal area (probably 1 muF approximately 1 cm2 actual area). A new mounting technique that virtually eliminates edge damage yielded resistances up to 78,000 omega muF for rabbit bladder, and resistances for amphibian skin and bladder much higher than those usually reported. This technique made it possible to observe a transport-related conductance pathway, and a close correlation between transepithelial conductance (G) and short-circuit current (Isc) in these tight epithelia. G and Isc were increased by mucosal (Na+) [Isc approximately 0 when (Na+) approximately 0], aldosterone, serosal (HCO-3) and high mucosal (H+); were decreased by amiloride, mucosal (Ca++), ouabain, metabolic inhibitors and serosal (H+); and were unaffected by (Cl-) and little affected by antidiuretic hormone (ADH). Physiological variation in the rabbits' dietary Na+ intake caused variations in bladder G and Isc similar to those caused by the expected in vivo changes in aldosterone levels. The relation between G and Isc was the same whether defined by diet changes, natural variation among individual rabbits, or most of the above agents. A method was developed for separately resolving conductances of junctions, basolateral cell membrane, and apical cell membrane from this G--Isc relation. Net Na+ flux equalled Isc. Net Cl- flux was zero on short circuit and equalled only 25% of net Na+ flux in open circuit. Bladder membrane fragments contained a Na+-K+-activated, ouabain-inhibited ATPase. The physiological significance of Na+ absorption against steep gradients in rabbit bladder may be to maintain kidney-generated ion gradients during bladder storage of urine, especially when the animal is Na+-depleted.
通过对兔膀胱进行体外实验，我们重新评估了传统观点，即哺乳动物的膀胱缺乏离子转运机制。由于折叠上皮中实际膜面积与标称膜面积的比值是可变的且难以估计，我们将膜特性标准化为顶端膜电容，而非标称面积（可能1μF约等于1cm²实际面积）。一种几乎消除边缘损伤的新固定技术，使兔膀胱的电阻高达78,000Ω·μF，两栖类皮肤和膀胱的电阻比通常报道的要高得多。该技术使得观察与转运相关的电导途径以及这些紧密上皮中的跨上皮电导（G）与短路电流（Isc）之间的密切相关性成为可能。G和Isc可被黏膜（Na⁺）[当（Na⁺）约为0时，Isc约为0]、醛固酮、浆膜（HCO₃⁻）和高浓度黏膜（H⁺）升高；可被氨氯吡脒、黏膜（Ca²⁺）、哇巴因、代谢抑制剂和浆膜（H⁺）降低；不受（Cl⁻）影响，且受抗利尿激素（ADH）影响较小。兔饮食中Na⁺摄入量的生理变化导致膀胱G和Isc的变化，类似于醛固酮水平预期的体内变化所引起的变化。无论是由饮食变化、个体兔之间的自然变异还是上述大多数试剂所定义，G和Isc之间的关系都是相同的。开发了一种方法，可从这种G - Isc关系中分别解析连接、基底外侧细胞膜和顶端细胞膜的电导。净Na⁺通量等于Isc。在短路时净Cl⁻通量为零，在开路时仅等于净Na⁺通量的25%。膀胱膜碎片含有一种Na⁺ - K⁺激活、哇巴因抑制的ATP酶。兔膀胱中逆陡峭梯度吸收Na⁺的生理意义可能是在膀胱储存尿液期间维持肾脏产生的离子梯度，尤其是当动物缺Na⁺时。
