McCaa R E
Prog Biochem Pharmacol. 1980;17:29-35.
In conscious sodium-deficient dogs, beta-adrenergic blockade with propranolol and angiotensin II receptor blockade with an angiotensin II inhibitory analogue reduced arterial blood pressure and increased urinary sodium excretion significantly, but the hypotensive and natriuretic response was considerably greater during inhibition of angiotensin I converting enzyme with captopril. Angiotensin II infusion (3 ng/kg/min) into sodium-deficient dogs maintained on captopril administration restored arterial blood pressure, urinary sodium excretion, and plasma aldosterone concentration to levels that existed in untreated sodium-deficient dogs. This indicates that the hypotensive and natriuretic actions of captopril are due to the inhibition of angiotensin II formation and not to the accumulation of the vasodepressor peptide, bradykinin.
在清醒的缺钠犬中,普萘洛尔进行β-肾上腺素能阻滞以及使用血管紧张素II抑制类似物进行血管紧张素II受体阻滞可显著降低动脉血压并增加尿钠排泄,但在用卡托普利抑制血管紧张素I转换酶期间,降压和利钠反应要大得多。向持续给予卡托普利的缺钠犬输注血管紧张素II(3 ng/kg/分钟)可使动脉血压、尿钠排泄和血浆醛固酮浓度恢复到未治疗的缺钠犬的水平。这表明卡托普利的降压和利钠作用是由于抑制了血管紧张素II的形成,而不是由于血管舒张肽缓激肽的蓄积。