左旋硝基精氨酸诱导高血压大鼠心肌肥大

一氧化氮合酶（ＮＯＳ）抑制剂Ｎ－左旋硝基精氨酸（Ｎ－ＬＮＡ）诱导持续性高血压大鼠１２只，随机分成２组测右颈动脉压，ＮＯ代谢物亚硝酸盐（ＮＯ２）浓度，心肌组织胶原蛋白含量及丝裂活化蛋白激酶（ＭＡＰＫ）活性，观察左心室心肌病理变化，发现与高血压比较，自然归组大鼠动脉血完全逆转（Ｐ〈０．０１）；ＮＯ２水平及ＭＡＰＫ活性轻度逆转，但均未达到正常对照组水平（Ｐ〈０．０１），胶原蛋白含量，心脏及左心室相对重量

DEVELOPMENT OF MYOCARDIAL HYPERTROPHY IN HYPERTENSIVE RATS INDUCED BY N OMEGA NITRO L ARGININE

In order to evaluate the mechanism on development of myocardial hypertrophy in L arginine analogue N omega nitro L arginine(LNA) induced sustained arterial hypertension (SAH),we tested the heart body weight ratio(HWR),left ventricle heart weight ratio(LWR),arterial blood pressure(ABP),left ventricular tissue content of collagen(CC),activity of tissue MAPK,serum concentration of metabolite of NO nitrate (NO - 2) in group (1) control:7 male 16 week old normotensive Wistar rats, 12 male 8 week old Wistar rats were treated with LNA(7 5mg/kg,2/d,ip) for 4 weeks,then divided into group (2) hypertensive (HT):6 SAH rats,(3) natural regressive (NR):6 SAH rats observed for 4 weeks after withdrawal of LNA.In addition,we also examined the myocardial pathomorphologic changes.In group HT compared with NR,we found a decrease in serum NO - 2 ( P <0 05),significant increases in ABP and in activity of MAPKs.No significant differences were found in HWR,LWR and CC.In group NR,as compared with control,we discovered significant increases in HWR, LWR,CC, MAPK activity, and a significant decrease in serum NO - 2( P <0 01). These data suggest that the myocardial hypertrophy in SAH induced by LNA may be related to the activation of MAPK via the decrease in production of nitric oxide.The myocardial fibrosis is independent of the level of the arterial blood pressure.