Natochin Iu V, Kanashkina T A, Shakhmatova E I, Bespalova Zh D, Mordvintsev D Iu, Poliak Ia L
Eksp Klin Farmakol. 2008 Mar-Apr;71(2):32-5.
Experiments on rats showed that the intramuscular injections of arginine-vasotocin (AVT), 1-deamino-arginine-vasotocin (1dAVT) or 1-deamino-1-monocarba-arginine-vasotocin (1dlmcAVT) at a dose of 5 x 10(-11) mole per 100 g body weight increase renal excretion of Na+, K+, and Mg2+. Antagonist of V1 receptors (OPC-21268) decreases the effect of 1dAVT nonapeptides on renal excretion of the studied ions. A model of VIb-receptor is constructed and a correlation is shown between the energy of interaction of the V1b-receptor and the natriuretic effect of the studied vasotocin analogs.
对大鼠的实验表明，以每100克体重5×10⁻¹¹摩尔的剂量肌肉注射精氨酸血管加压素（AVT）、1-脱氨基-精氨酸血管加压素（1dAVT）或1-脱氨基-1-单碳-精氨酸血管加压素（1dlmcAVT），会增加肾脏对Na⁺、K⁺和Mg²⁺的排泄。V1受体拮抗剂（OPC-21268）会降低1dAVT九肽对所研究离子肾脏排泄的影响。构建了VIb受体模型，并显示了V1b受体相互作用能量与所研究的血管加压素类似物的利钠作用之间的相关性。
