Selig S E, Anderson W P, Korner P I, Casley D J
J Hypertens. 1983 Aug;1(2):153-8. doi: 10.1097/00004872-198308000-00007.
The responses to 48 h of renal artery stenosis were compared in uninephrectomized, chronically-instrumented dogs with or without inhibition of angiotensin II (AII) formation by enalapril. Mean arterial pressure rose by an average of 29.9 mmHg (s.e.m. 3.5) in untreated dogs and by 14.5 mmHg (s.e.m. 2.8) in enalapril-treated dogs over the two days of stenosis. Renal artery stenosis reduced glomerular filtration rate (GFR) by 49% (s.e.m. 9) in untreated dogs and by 86% (s.e.m. 8) in enalapril-treated dogs. Compared to untreated dogs, enalapril-treated dogs also had lower renal artery pressure distal to the stenosis, drank less water and had larger rises in plasma K+ following renal artery stenosis. There were no differences in renal blood flow or urinary Na+ excretion in the two groups of dogs. Thus blockade of AII production did not prevent hypertension occurring in response to renal artery stenosis, but the rise in blood pressure was only about half that which occurred in normal dogs and GFR was much more severely reduced.
对单侧肾切除、长期植入仪器的犬,比较了在有或没有依那普利抑制血管紧张素II(AII)形成的情况下,肾动脉狭窄48小时的反应。在狭窄的两天内,未治疗犬的平均动脉压平均升高29.9 mmHg(标准误3.5),依那普利治疗犬的平均动脉压升高14.5 mmHg(标准误2.8)。肾动脉狭窄使未治疗犬的肾小球滤过率(GFR)降低49%(标准误9),使依那普利治疗犬的肾小球滤过率降低86%(标准误8)。与未治疗犬相比,依那普利治疗犬在狭窄远端的肾动脉压力也更低,饮水更少,肾动脉狭窄后血浆K+升高幅度更大。两组犬的肾血流量或尿Na+排泄没有差异。因此,阻断AII生成并不能预防肾动脉狭窄引起的高血压,但血压升高仅约为正常犬的一半,而GFR降低更为严重。