Antihypertensive Effect of Total Flavonoid Fraction of Astragalus complanatus in Hypertensive Rats

Jing-Xin Li；Bing Xue；Qiang Chai；Zhi-Xiang Liu；Ai-Ping Zhao；Lian-Bi Chen

Astragalus complanatus ； total flavonoid ； hypertension ； antihypertensive effect ； hemodynamics

The Chinese Journal of Physiology

48卷2期（2005 / 06 / 01）

101 - 106

英文

The purpose of the present study was to quantify the antihypertensive effect of the total flavonoid (TF), extracted from the seed of Astragalus complanatus R. Brown, and to observe its effect on the renin-angiotensin system (RAS) in both renal hypertensive rats (RHR) and spontaneously hypertensive rats (SHR). RHR were created by the two-kidney one clip (2K1C) method. Systolic blood pressure was measured in conscious rats by the tail-cuff method. Plasma angiotensin Ⅱ (AngⅡ) and plasma renin activity (PRA) were measured with radioimmunoassay at 60 min after drug administration. The effects of TF on cardiac hemodynamics were also recorded in anesthetized RHR and SHR. TF was given by oral administration in low dose (100 mg/kg) and high dose (200 mg/kg) respectively. Compared to preadministration control, TF induced an obvious decrease in systolic blood pressure in conscious normotensive Wistar rat, RHR and SHR. In the three groups the systolic blood pressure reached the lowest value at 60 min after TF. TF also induced a significant decrease in blood pressure in anesthetized RHR and SHR. At 60 min after treatment of TF, mean arterial pressure in high dose group (200 mg/kg) was decreased by 17% in RHR and by 17% in SHR respectively (P＜0.01). The depressor effect of TF lasted for at least 60 min. Cardiac output, heart rate and ±dp/dtmax did not change. Conversely, total peripheral resistance was significantly decreased. The decrease in plasma AngⅡ was found in both RHR and SHR. On the contrary, PRA increased at the same time. These findings suggested that TF is effective in reducing blood pressure in both RHR and SHR. The antihypertensive action of TF was attributed to a decrease in TPR secondary to a decrease in plasma concentration of AngⅡ caused by TF.

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