Fejes-Tóth G, Zahajszky T, Filep J
Am J Physiol. 1983 Feb;244(2):F205-9. doi: 10.1152/ajprenal.1983.244.2.F205.
Inhibition of the renin-angiotensin system with saralasin or with SQ 20,881 was used to examine a possible interaction between endogenous angiotensin II and antidiuretic hormone in renal water excretion. In sodium-depleted anesthetized rats undergoing water diuresis, neither saralasin nor SQ 20,881 had any significant effect on water excretion. Both drugs, however, markedly potentiated the antidiuretic response to arginine vasopressin. A similarly enhanced antidiuresis was also observed when the renal response to 1-desamino-8-D-arginine vasopressin was investigated in the presence or absence of saralasin. There were no significant changes in sodium or potassium excretion or in glomerular filtration rate in any of the groups studied. Neither was there any interaction of the drugs with relation to blood pressure. These results seem to indicate that endogenous angiotensin II is capable of antagonizing the hydroosmotic effect of antidiuretic hormone.
使用沙拉新或SQ 20,881抑制肾素-血管紧张素系统,以研究内源性血管紧张素II与抗利尿激素在肾脏水排泄过程中可能存在的相互作用。在进行水利尿的钠缺乏麻醉大鼠中,沙拉新和SQ 20,881对水排泄均无显著影响。然而,这两种药物均显著增强了对精氨酸加压素的抗利尿反应。当在有或没有沙拉新存在的情况下研究肾脏对1-去氨基-8-D-精氨酸加压素的反应时,也观察到了类似增强的抗利尿作用。在所研究的任何组中,钠或钾排泄以及肾小球滤过率均无显著变化。药物与血压之间也没有相互作用。这些结果似乎表明,内源性血管紧张素II能够拮抗抗利尿激素的水渗透作用。