Orce G G, Castillo G A
Comp Biochem Physiol C Comp Pharmacol Toxicol. 1986;84(1):139-44. doi: 10.1016/0742-8413(86)90179-9.
Captopril (CA), a specific inhibitor of kininase II, did not alter osmotic water permeability (Posm) when present in the mucosal bath of the urinary bladder isolated from the toad Bufo arenarum at a concentration of 2.3 X 10(-3) M. This treatment, however, caused a 65% enhancement in the increase in Posm following serosal exposure to vasopressin, oxytocin or theophylline, agents that increase intracellular cyclic AMP levels. The effect of captopril was prevented by procedures that reduce the kallikrein (KK)-like alkaline esterase activity present in the bladder (such as simultaneous exposure to 2.3 X 10(-5) M aprotinin, or pretreatment of the toads with 0.1 N NaCl for several days before the experiment) or by replacing the mucosal bath with fresh solution of identical composition after exposure to captopril. In contrast, changing the serosal bath did not alter the effect of the drug. These results are consistent with an effect of CA at a step beyond cAMP generation, and suggest it is mediated by release of a soluble factor, probably a kinin, into the mucosal bath. These observations, together with data previously published, suggest that the KK-kinin system may participate in the control of epithelial water and electrolyte permeability in the toad bladder. In particular, under environmental stress, it may become important in the regulation of the animal's extracellular fluid volume, thus exhibiting an adaptive value.
卡托普利（CA）是激肽酶II的特异性抑制剂，当以2.3×10⁻³ M的浓度存在于从蟾蜍Bufo arenarum分离的膀胱黏膜浴中时，它不会改变渗透水通透性（Posm）。然而，这种处理导致在浆膜暴露于血管加压素、催产素或茶碱（这些物质会增加细胞内环状AMP水平）后，Posm的增加提高了65%。降低膀胱中存在的激肽释放酶（KK）样碱性酯酶活性的操作（如同时暴露于2.3×10⁻⁵ M抑肽酶，或在实验前用0.1 N NaCl对蟾蜍进行预处理数天），或在暴露于卡托普利后用相同成分的新鲜溶液替换黏膜浴，均可阻止卡托普利的作用。相反，更换浆膜浴不会改变药物的作用。这些结果与CA在cAMP生成之后的一个步骤中的作用一致，并表明它是由一种可溶性因子（可能是一种激肽）释放到黏膜浴中介导的。这些观察结果与先前发表的数据一起表明，KK-激肽系统可能参与蟾蜍膀胱上皮水和电解质通透性的控制。特别是在环境应激下，它可能在调节动物细胞外液体积方面变得很重要，从而表现出一种适应性价值。
