前胡丙素对高血压大鼠血压及犬血管阻力的影响

目的　观察前胡丙素(pra C)的降压及对外周血管阻力的影响。方法　在肾型高血压大鼠模型与正常血压大鼠用尾容积法测血压。用RDB III型输液泵连接于麻醉杂种犬,以控制血流量与压力法直接测定锥动脉、冠脉左旋支、股动脉的阻力。结果　pra-C 20 mg·kg^-1·d^-1 ig给药3 0d对肾性高血压大鼠(RHR)降压峰值时间为6h ,从(213±10 )mmHg降至(144.0±1.5)mmHg,降低原水平30% ,持续至20h。pra-C分别以100 μg·kg^-1 及20 μg·kg^-1与pra-E 20 μg·kg^-1iv可降低上述血管的阻力,减慢心率,降低阻力呈剂量相关。结论　pra-C有降压作用,降低犬外周动脉阻力,增加小鼠耐缺氧时间。

EFFECTS OF PRAERUPTORIN C ON BLOOD PRESSURE IN HYPERTENSIVE RATS AND VASCULAR RESISTANCE IN DOGS

AIM To study the effects of praeruptorin C (pra-C) on conscious renovascular hypertensive and normotensive rats and the vascular resistance of vertebral, left circumflex coronary and femoral artery in anesthetized dogs. METHODS Hypertensive rats were obtained after the left renal arteries of normal rats were narrowed to 0.2 mm diameter by silver clips. Systotic blood pressure was measured by the tail cuff method. Measurements of systolic blood pressure were carried out before administration of the drug as well as 2, 4, 6, 20 and 24 h after drug administration. Hypertensive and normotensive rats were given pra-C 20 mg·kg^-1 orally once daily for 30 days. Using sum of squares of deviations from the mean data were analysed and compared with the controls before and after drug administration. Nifedipine was compared with pra-C on the same dose. Vascular resistance were measured on the constant rate perfusion preparation. RESULTS Pra-C reduced significantly the blood pressure in hypertensive and normotensive rats. The peak effect of pra-C and nifedipine were observed 4-6 h and 2-4 h after drug administration respectively. The hypotensive effect of pra-C was similar to that of the nifedipine at the same dose, but the action of oral pra-C lasted longer than that of nifedipine. The blood pressure lowering effect of pra-C after 3 weeks (20-30 d) of treatment is even more potent than at the beginning (1-15 d) of the trial. This indicates that there is no acquired tolerance in blood pressure. Pra-C 20 μg·kg^-1 or 100 μg·kg^-1 iv in dogs produced distinct fall of vascular resistance in vertebral, left circumflex coronary and femoral arterial resistance. Peak of effect was observed 50-60 min after drug administration. Reduction in vertebral vascular resistance was much more than that of the other two arteries. However, the effects recovered to its initial values 70 min after medication. The medication caused a reduction of systolic blood presure and slowing of heart rate. Pra-C is better than nifedipine in slowing heart rate. Pra-C prolonged the tolerance to anoxia in mice. CONCLUSION These results suggest that the antihypertensive action of pra-C may be due to peripheral vasodilation. It is reasonable to anticipate that pra-C may be an agent of choice in the treatment of hypertensive encephalopathy.