Suzuki H, Fujimaki M, Nakane H, Saito I, Takeshita E, Saruta T
Nephron. 1985;39(3):244-9. doi: 10.1159/000183379.
Captopril (SQ14,225), an orally administered angiotensin converting enzyme inhibitor, was given to 8 patients with idiopathic edema, in order to study the role of the renin-angiotensin-aldosterone system in orthostatic sodium and water retention. Compared to 5 normal subjects, patients with idiopathic edema showed significantly greater reduction in water and sodium excretion, and greater increment in plasma aldosterone and plasma renin activity, in the upright posture. Captopril significantly restored water and sodium excretion, attenuated the increment in plasma aldosterone, and enhanced the rise in plasma renin activity in patients with idiopathic edema. The effects of captopril on these variables were not remarkable in normal subjects. These results suggest that an enhanced response of the renin-angiotensin-aldosterone system to standing plays an important role in the pathophysiology of idiopathic edema.
卡托普利(SQ14,225)是一种口服的血管紧张素转换酶抑制剂,为研究肾素 - 血管紧张素 - 醛固酮系统在体位性钠水潴留中的作用,对8例特发性水肿患者给予了该药。与5名正常受试者相比,特发性水肿患者在直立姿势下的水和钠排泄显著减少,血浆醛固酮和血浆肾素活性显著增加。卡托普利可显著恢复特发性水肿患者的水和钠排泄,减弱血浆醛固酮的增加,并增强血浆肾素活性的升高。卡托普利对这些变量的影响在正常受试者中并不显著。这些结果表明,肾素 - 血管紧张素 - 醛固酮系统对站立的反应增强在特发性水肿的病理生理学中起重要作用。