Mann J F, Rascher W, Schömig A, Dietz R
Klin Wochenschr. 1978;56 Suppl 1:67-70. doi: 10.1007/BF01477455.
Brattleboro rats homozygous for hypothalamic hereditary diabetes insipidus (DI rats) were used to investigate the following questions: a) Do exogenous and endogenous angiotensin II (AII) have an antidiuretic effect in diabetes insipidus? b) Does AII mediate the antidiuresis induced by furosemide? The following results were obtained: 1. AII (5 mg/kg s.c. in oil) and furosemide (50 mg/kg i.p.) decreased urine flow and increased urinary sodium excretion. Furosemide led to a two-fold increase of AII plasma concentrations and a decrease of plasma sodium levels. 2. SQ 14 225 (2 x 2.5 mg/kg p.o.), an angiotensin I-converting enzyme inhibitor, led to an increase of urine flow and to a slightly elevated urinary sodium excretion. 3. When the formation of AII was blocked by SQ 14 225 (2 x 2.5 mg/kg p.o.), AII plasma concentrations were 2.5-fold decreased, but furosemide still reduced urine flow. We conclude that plasma AII might have an antidiuretic action in DI rats. However, AII does not mediate the antidiuresis induced by furosemide.
使用下丘脑遗传性尿崩症纯合子的布拉德福德大鼠（DI大鼠）来研究以下问题：a）外源性和内源性血管紧张素II（AII）在尿崩症中是否具有抗利尿作用？b）AII是否介导速尿诱导的抗利尿作用？获得了以下结果：1. AII（5mg/kg皮下注射于油中）和速尿（50mg/kg腹腔注射）减少尿流量并增加尿钠排泄。速尿导致AII血浆浓度增加两倍，血浆钠水平降低。2. 血管紧张素I转换酶抑制剂SQ 14 225（2×2.5mg/kg口服）导致尿流量增加，尿钠排泄略有升高。3. 当AII的形成被SQ 14 225（2×2.5mg/kg口服）阻断时，AII血浆浓度降低2.5倍，但速尿仍减少尿流量。我们得出结论，血浆AII可能在DI大鼠中具有抗利尿作用。然而，AII并不介导速尿诱导的抗利尿作用。
