摘要
目的 观察自发性高血压大鼠肾脏内一氧化氮合酶(NOS)活性变化 ,以探讨高血压病的发病机制 .方法 采用 3H-精氨酸转变成 3H-胍氨酸方法测定 NOS活性 .结果 自发性高血压大鼠 (SHR)肾蛋白内神经型 NOS(n NOS)活性(2 1.9± 7.4) k Bq· g- 1明显低于 Wistar Kyoto(WKY)大鼠(4 .32± 9.3) k Bq·g- 1 ,P<0 .0 5 .在乙酰胆碱 (Ach)刺激后 ,SHR肾内内皮型 NOS(e NOS)活性为 (6 7.3± 14.6 ) k Bq·g- 1 ,而 WKY肾内 e NOS则为 (85 .7± 2 3.8) k Bq· g- 1 ,SHR也显著低于 WKY(P<0 .0 5 ) .结论 n NOS和 e
AIM To investigate the change of activity of the nitric oxide synthase (NOS) in the kidney of spontaneously hypertensive rats and the role in the mechanism of hypertension. METHODS Activity of NOS was assayed by monitoring the convertion of 3H arginine to 3H citruline. RESULTS The activity of neural type of NOS (nNOS) in the kidney protein of spontaneously hypertensive rats (SHR) was much lower than that in Wistar Kyoto (WKY)(activity of nNOS: (21.9±7.4) kBq·g -1 and (43.2±9.3) kBq·g -1 for SHR and WKY,respectively( P <0.05). After the stimulation by the acetylcholine(Ach)1, activity of endothelia type of NOS (eNOS) in SHR was also lower than that in WKY(activity of eNOS: (67.3±14.6) kBq·g -1 and (8.57±23.8) kBq·g -1 for SHR and WKY, respectively( P <0.05). CONCLUSION The insufficient activity of nNOS and eNOS could play important role in the genesis and development of hypertension.
出处
《第四军医大学学报》
2000年第10期1271-1272,共2页
Journal of the Fourth Military Medical University
关键词
高自压
一氧化氮合酶
肾脏
hypertension
nitric oxide synthase
kidney