Miyamori I, Brown M J, Dollery C T
Clin Exp Hypertens (1978). 1980;2(6):935-45. doi: 10.3109/10641968009037152.
The effect of an oral angiotensin I converting enzyme inhibitor, SQ 14225 (Captopril) on blood pressure and plasma renin activity (PRA) was studied in deoxycorticosterone-salt (DOCA/salt) hypertensive rats. Intraperitoneal (ip) injection of captopril (1 mg/kg) produced a significant fall in systolic blood pressure (23.4 +/- 5.0 mm Hg, p < 0.001) whereas no significant change in blood pressure occurred in control rats. Indomethacin (IDM) (2.5 mg/kg ip) pretreatment significantly (p < 0.01) attenuated the hypotensive action of captopril in DOCA/salt rats. PRA was markedly suppressed in DOCA/salt rats (0.3 +/- 0.1 ng/ml/hr) when compared with the normotensive controls (4.4 +/- 2.2 ng/ml/hr, p < 0.001) at baseline. Captopril induced a significant rise in PRA in both groups of rats. These responses were not significantly altered by IDM pretreatment. The hypotensive effect of captopril in the DOCA/salt model may be mediated by prostaglandins since their synthesis is inhibited by indomethacin.
在脱氧皮质酮盐(DOCA/盐)高血压大鼠中研究了口服血管紧张素I转换酶抑制剂SQ 14225(卡托普利)对血压和血浆肾素活性(PRA)的影响。腹腔注射卡托普利(1毫克/千克)可使收缩压显著下降(23.4±5.0毫米汞柱,p<0.001),而对照大鼠的血压无显著变化。吲哚美辛(IDM)(2.5毫克/千克腹腔注射)预处理显著(p<0.01)减弱了卡托普利对DOCA/盐大鼠的降压作用。与正常血压对照组(4.4±2.2纳克/毫升/小时,p<0.001)相比,DOCA/盐大鼠在基线时的PRA明显受到抑制(0.3±0.1纳克/毫升/小时)。卡托普利使两组大鼠的PRA显著升高。吲哚美辛预处理并未显著改变这些反应。卡托普利在DOCA/盐模型中的降压作用可能由前列腺素介导,因为吲哚美辛可抑制其合成。