Natochin Iu V, Kanashkina T A, Mordvintsev D, Shakhmatova E I
Ross Fiziol Zh Im I M Sechenova. 2007 Jun;93(6):625-34.
In experiments on non-anesthetized female Wistar rats, it has been shown that injection of 1-deamino-arginine-vasotocin (1dAVT) increases sodium excretion and solute-free water reabsorption. Antagonists of V1-receptors (OPC-31260, Otsuka Pharmaceutical Co., Ltd., Japan) eliminates the effect water reabsorption whereas antagonist of V1-receptors (OPC-21268, Otsuka Pharmaceutical Co., Ltd., Japan) decreases the 1dAVT-dependent increase of Na+ and water excretion. A model of V1-receptors an a supposed topography of their interaction with 1dAVT are constructed.
在对未麻醉的雌性Wistar大鼠进行的实验中，已表明注射1-脱氨基-精氨酸-血管加压素（1dAVT）会增加钠排泄和无溶质水重吸收。V1受体拮抗剂（OPC-31260，日本大冢制药有限公司）消除了水重吸收的作用，而V1受体拮抗剂（OPC-21268，日本大冢制药有限公司）降低了1dAVT依赖性的钠和水排泄增加。构建了V1受体模型及其与1dAVT相互作用的假定拓扑结构。
