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。
