Kachadorian W A, Muller J, Ellis S J
Am J Physiol. 1986 May;250(5 Pt 2):F845-9. doi: 10.1152/ajprenal.1986.250.5.F845.
Toad urinary bladders were subjected to sequential 30-min stimulation with antidiuretic hormone (ADH) followed by 30-min hormone washout over 4 h in the absence of a transmural osmotic gradient. Immediately thereafter, during test stimulation with hormone in the presence of a transmural gradient, transbladder water flow was profoundly inhibited, but intra(luminal)membrane particle aggregates, presumed markers of luminal membrane water permeability, were as numerous as in fully responsive controls. The protocol followed was designed to eliminate any distorting effect of prior water flow on cytoplasmic organization and to equalize, for both experimental and control tissues, the time of aggregate presence in the luminal membrane during final test stimulation. On the assumption that cytoplasmically stored and/or newly synthesized aggregates would be unaffected by the protocol followed, these observations appear to be consistent with the view that bladder refractoriness to prolonged ADH treatment may involve regulation of tissue water permeability at a resistance distal to the luminal membrane.
在不存在跨膜渗透梯度的情况下，对蟾蜍膀胱进行连续30分钟的抗利尿激素（ADH）刺激，随后在4小时内进行30分钟的激素洗脱。此后立即，在存在跨膜梯度的情况下用激素进行测试刺激时，经膀胱水流受到显著抑制，但腔内（膜内）颗粒聚集体（推测为腔膜水通透性的标志物）的数量与完全反应性对照中的数量一样多。所遵循的实验方案旨在消除先前水流对细胞质组织的任何扭曲作用，并使实验组织和对照组织在最终测试刺激期间腔膜中聚集体存在的时间相等。假设细胞质中储存和/或新合成的聚集体不会受到所遵循方案的影响，这些观察结果似乎与以下观点一致，即膀胱对长期ADH治疗的不应性可能涉及在腔膜远端的阻力处对组织水通透性的调节。
