血管紧张素转换酶抑制剂MK 421、SA 446和卡托普利对清醒正常血压大鼠肾前列腺素E和激肽的影响。

Effects of angiotensin converting enzyme inhibitors MK 421, SA 446 and captopril on renal prostaglandin E and kinins in conscious normotensive rats.

作者信息

Yasujima M, Abe K, Tanno M, Kohzuki M, Kasai Y, Kanazawa M, Omata K, Sato M, Takeuchi K, Yoshinaga K

出版信息

Clin Exp Hypertens A. 1987;9(2-3):401-4. doi: 10.3109/10641968709164205.

DOI:10.3109/10641968709164205

Abstract

Angiotensin converting enzyme inhibition by MK 421, SA 446 or captopril (6 mg/kg/day ip) for up to 6 days induced significant fall in systolic blood pressure and plasma angiotensin II concentration. The hypotensive effect was greater in sodium depleted rats than in sodium repleted rats. The hypotensive effect was also accompanied by increased excretion of urinary prostaglandin E2, however the levels of urinary prostaglandin E2 in sodium repleted rats were not different from those in sodium depleted rats. Urinary kinin excretion was increased during infusion of MK 421, SA 446 or captopril in sodium depleted rats, whereas no significant change was found in sodium repleted rats. Thus the present results suggest that renal prostaglandin E system may not be essential for the hypotensive effect of these inhibitors. In addition, the greater hypotensive effect of these inhibitors in sodium depleted rats may be in part due to stimulated renal kinin system.

摘要

MK 421、SA 446或卡托普利（6毫克/千克/天，腹腔注射）抑制血管紧张素转换酶长达6天，可导致收缩压和血浆血管紧张素II浓度显著下降。缺钠大鼠的降压作用比补钠大鼠更强。降压作用还伴有尿前列腺素E2排泄增加，然而，补钠大鼠的尿前列腺素E2水平与缺钠大鼠并无差异。在缺钠大鼠输注MK 421、SA 446或卡托普利期间，尿激肽排泄增加，而补钠大鼠未发现显著变化。因此，目前的结果表明，肾前列腺素E系统可能对这些抑制剂的降压作用并非必不可少。此外，这些抑制剂在缺钠大鼠中更强的降压作用可能部分归因于肾激肽系统的激活。