Hashimoto H, Hiwada K, Kokubu T
Clin Exp Hypertens A. 1983;5(3):429-45. doi: 10.3109/10641968309069498.
To evaluate the difference of the blood pressure regulating mechanisms of chronic (12-14 weeks) one-kidney, one-clip (1K-1C) and chronic two-kidney, one-clip (2K-1C) hypertensive rats, we administered captopril, captopril plus indomethacin, and indomethacin to the rats. Pretreatment values of plasma renin concentration, plasma aldosterone concentration and urinary kallikrein excretion were significantly higher in 2K-1C than in 1K-1C hypertensive rats. Captopril-induced blood pressure reduction was greater in 2K-1C than in 1K-1C hypertensive rats. When captopril was administered to the rats treated with indomethacin, captopril-induced blood pressure reduction was attenuated only in 2K-1C hypertensive rats. Indomethacin produced renal impairment and further raised the blood pressure in 1K-1C hypertensive rats, but did not in 2K-1C hypertensive rats. These results suggest that the renin-angiotensin system functions to maintain high blood pressure more predominantly in chronic 2K-1C than in 1K-1C hypertensive rats. The renal kallikrein-kinin system is suppressed in chronic 1K-1C hypertensive rats but not in 2K-1C hypertensive rats. The renal prostaglandin system is more important for regulating the renal circulation in chronic 1K-1C than in 2K-1C hypertensive rats.
为评估慢性(12 - 14周)单肾单夹(1K - 1C)和慢性双肾单夹(2K - 1C)高血压大鼠血压调节机制的差异,我们给大鼠施用了卡托普利、卡托普利加吲哚美辛以及吲哚美辛。2K - 1C高血压大鼠的血浆肾素浓度、血浆醛固酮浓度和尿激肽释放酶排泄的预处理值显著高于1K - 1C高血压大鼠。卡托普利诱导的血压降低在2K - 1C高血压大鼠中比在1K - 1C高血压大鼠中更大。当给用吲哚美辛处理的大鼠施用卡托普利时,卡托普利诱导的血压降低仅在2K - 1C高血压大鼠中减弱。吲哚美辛在1K - 1C高血压大鼠中产生肾损害并进一步升高血压,但在2K - 1C高血压大鼠中则不然。这些结果表明,肾素 - 血管紧张素系统在维持慢性2K - 1C高血压大鼠的高血压方面比在1K - 1C高血压大鼠中发挥更主要的作用。慢性1K - 1C高血压大鼠的肾激肽释放酶 - 激肽系统受到抑制,而2K - 1C高血压大鼠则不然。肾前列腺素系统在调节慢性1K - 1C高血压大鼠的肾循环方面比在2K - 1C高血压大鼠中更重要。