Yuasa S, Urakabe S, Kimura G, Shirai D, Takamitsu Y
Biochim Biophys Acta. 1975 Dec 1;413(2):277-82. doi: 10.1016/0005-2736(75)90112-1.
Osmotic water movement across the toad urinary bladder in response to both vasopressin and cyclic AMP was inhibited by 10(-5) to 10(-4) M colchicine on the serosal but not on the mucosal side. This inhibitory effect was found to be time- and dose-dependent. Colchicine alone did not change basal osmotic flow and a baseline of the short-circuit current (Isc) and also did not affect a vasopressin-induced rise of the Isc. The inhibitory effect was not prevented by the addition of pyruvate. The osmotic water movement produced by 360 mM Urea (mucosal), 360 mM mannitol (serosal) or 2 mug/ml amphotericin B (mucosal), was not affected by 10(-4) M colchicine. These results suggest that colchicine inhibits some biological process subsequent to the formation of cyclic AMP except a directional cytoplasmic streaming process where microtubules may be involved.
10(-5)至10(-4)M秋水仙碱可抑制蟾蜍膀胱黏膜侧对血管加压素和环磷酸腺苷(cAMP)产生的渗透性水移动,但浆膜侧不受影响。这种抑制作用具有时间和剂量依赖性。单独使用秋水仙碱不会改变基础渗透流和短路电流(Isc)的基线,也不会影响血管加压素诱导的Isc升高。添加丙酮酸不能阻止这种抑制作用。360mM尿素(黏膜侧)、360mM甘露醇(浆膜侧)或2μg/ml两性霉素B(黏膜侧)产生的渗透性水移动不受10(-4)M秋水仙碱的影响。这些结果表明,秋水仙碱在环磷酸腺苷形成后抑制了某些生物学过程,但不包括可能涉及微管的定向细胞质流动过程。