本研究以自發性高血壓大白鼠為動物模式,於飲食和飲水中分別添加1% 和0.9% 之氯化鈉,控制組供應正常配方飼料(SC組),實驗組添加0.5%(S1組)及1%(S2組)之大豆蛋白質水解產物,結果發現:S1和S2組收縮壓和平均血壓上升趨勢皆較SC組緩慢;S1和S2組血漿血管收縮素轉換酶活性顯著較SC組低;三組自發性高血壓大白鼠組織血管收縮素轉換酶活性皆以主動脈中最高,而添加大豆蛋白質水解產物的組別僅在心臟血管收縮素轉換酶活性較未添加組別低;大豆蛋白質水解產物的添加對血脂質和血漿電解質濃度並未造成影響。病理分析中,所有組別組動物之左心室壁厚度皆有增厚的情形發生。本研究中並進一步將大豆蛋白質水解產物以不同濃度甲醇溶液劃分為五個部分(I, 0%;II, 6.25%;III, 12.5%;IV, 25%;V, 50%),體外實驗中發現以劃分II之IC50最低,但在強制經口投予實驗中則以劃分IV對血壓的影響最為明顯。綜合以上結果得知:自發性高血壓大白鼠長期攝取大豆蛋白質之酵素水解物並不會影響體內的電解質平衡,且可能藉由抑制體內血管收縮素轉換酶的活性來達到延緩血壓上升的效果。
The aim of this study is to investigate the antihypertensive and ACE (angiotensin converting enzyme) inhibition effects of soy protein hydrolysate in spontaneously hypertenisve rats (SHR). Soy protein hydrolysate was prepared by peptic hydrolysis and was added in to the SHR feed (0% for SC, 0.5% for S1 and 1% for S2). 1% NaCl was added into the animal feed and 0.9% NaCl was added into the drinking water. Blood pressure, plasma and heart ACE activity of the S1 and S2 group were significantly lower than the control group at the end of the study and aorta, heart and lung ACE activity of the three SHR groups were significantly higher than the Wistar group. Soy protein hydrolysate had no significant effect on plasma lipids, electrolytes, left ventricular wall and aorta wall thickness . Futhermore, we isolated fraction I~V from soy protein hydrolysate by different concentration of methanol (I, 0%;II, 6.25%;III, 12.5%;IV, 2%;V, 50%). The in vitro study showed that fraction II had the lowest IC50. However, the in vivo study showed that fraction IV had the best depressor effect after an oral administration. These data suggest that soy protein hydrolysate can significantly retarded the development of hypertension in SHR by their ACE inhibitory effect in vivo.