伊贝沙坦对自发性高血压大鼠细胞钙离子转运蛋白的影响

目的观察在高血压发病过程中,主动脉血管平滑肌细胞Ca~(2+)转运蛋白活性的改变,阐明伊贝沙坦(IBT)降低血压与上述蛋白活性改变的相关性。方法选取16周龄健康雄性自发性高血压大鼠(SHR)16只,随机分为IBT组(8只)和SHR组(8只),另选健康雄性Wistar Kyoto大鼠8只为正常对照组(WKY组)。IBT组大鼠给予IBT 60 mg/(kg·d)加适量蒸馏水灌胃14周。观察给药前后大鼠尾动脉收缩压的变化,并检测胸主动脉平滑肌细胞Na~+-K~+ATP酶和Ca~(2+)Mg~(2+)-ATP酶的活性。结果与SHR组比较,给药14周后,IBT组和WKY组大鼠尾动脉收缩压明显降低;IBT组和WKY组大鼠血管平滑肌细胞Na~+-K~+-ATP酶和Ca~(2+)-Mg~(2+)ATP酶活性均明显升高(P0.05,P0.01)。Na~+-K~+-ATP酶和Ca~(2+)-Mg~(2+)-ATP酶活性与血压呈显著负相关(r=-0.446,r=-0.387,P0.01)。结论高血压的发病与细胞Ca~(2+)转运蛋白活性的改变有关。IBT干预14周可以改善SHR的血管平滑肌细胞Ca~(2+)转运蛋白活性。

Effects of irbesartan on cell calcium transport protein in spontaneously hypertensive rats

Objective To investigate changes of calcium transport protein activities of aortic smooth muscle cell in progress of hypertension,and to elucidate the relationship between blood-presurelowering effect of irbesartan and changes of this protein.Methods Sixteen 16-week-old SHR were randomized into irbesartan treated groupGBT group,n = 8) and distilled water group(SHR group,n = 8) ,and Wistar Kyoto rats(WKY,n = 8) served as normal controls.Irbesartan and appropriate amount of distilled water were administered respectively for 14 weeks by gavage.Blood pressure of caudal artery was examined before and after treatment,activities of Na~+-K~+-ATPase and Ca~(2+)-Mg~(2+)-ATPase of thoracic aorta smooth muscle cell were measured.Results After medication for 14 weeks,blood pressure in IBT group and WKY group was much lower than that in SHR group.Compared with SHR group,activities of Na~+-K~+-ATPase and Ca~(2+)-Mg~(2+)-ATPase of thoracic aorta smooth muscle cell were significantly higher in both IBT group and WKY group. Activities of Na~+-K~+-ATPase and Ca~(2+)-Mg~(2+)-ATPase of thoracic aorta smooth muscle cell were negatively correlated to blood pressure (r =— 0.446,r =— 0.387,P < 0.01).Conclusion The changes of calcium transport protein activities of aortic smooth muscle cell play an important role in the development of hypertension.Administration of Irbesartan for 14 weeks ameliorated effectively calcium transport protein activities of vascular smooth muscle cells.