摘要
目的 :研究自发性高血压大鼠 (SHR)肾脏 (L -精氨酸 /一氧化氮 )L -Arg/NO系统的改变及其与红细胞L -Arg转运的关系。方法 :检测 16周龄SHR、卡托普利治疗 4周的 16周龄SHR(CAP)和 16周龄WKY大鼠肾脏L -Arg转运、NOS活性、NO-2 和cGMP含量 ,红细胞L -Arg转运。结果 :SHR肾脏高低亲和L -Arg转运体的Vmax均低于WKY组 (P <0 .0 1,P <0 .0 5 ) ,Km值则无明显差异。NOS活性、NO-2 、cGMP含量分别较WKY组低35 .4%、36 .2 %和 85 .2 % (P <0 .0 5或P <0 .0 1)。CAP组高亲和L -Arg转运体的Vmax、NOS活性均高于SHR组(+ 90 % ,P <0 .0 1;+ 5 8.6 % ,P <0 .0 5 )。NOS活性与高亲和L -Arg转运体的Vmax呈正相关 ,r =0 .5 85 ,P <0 .0 5。红细胞L -Arg转运的改变与肾脏相似 ,SHR组的Vmax低于WKY组 (- 30 % ,P <0 .0 1) ,CAP组高于SHR组(+ 2 6 .5 % ,P <0 .0 1) ,Km值组间比较无明显差异。红细胞L -Arg转运的Vmax与肾脏高或低亲和L -Arg转运体的Vmax均呈正相关 ,r =0 .8434,P <0 .0 1(高亲和 )和r=0 .5 2 5 5 ,P <0 .0 5 (低亲和 )。结论 :SHR肾脏L -Arg/NO系统活动抑制 ,卡托普利治疗明显解除此抑制状态。肾脏L -Arg转运的改变与红细胞L -Arg转运的改变基本一致。
AIM: To investigate the changes of the renal L-arginine /nitric oxide pathway and the relationship of L-arginine transport between kidney and erythrocytes in spontaneously hypertensive rat (SHR). METHODS: Sixteen week old SHR, 16 week old SHR with captopril (CAP) treated for four weeks and 16 week old WKY rats were used in the experiment. L-arginine transport, NO synthase(NOS) activity, nitrite and cyclic GMP (cGMP) content were measured in renal tissue or erythrocytes. RESULTS: In the renal tissue, compared with that of WKY group, the Vmax of high-or low-affinity L-arginine transporter, NOS activity, NO - 2 and cGMP content of SHR group were significantly decreased ( P <0.01 or P <0.05). The Vmax of high-affinity L-arginine transporter and NOS activity of CAP group were significantly enhanced as compared with SHR group (+90%, P <0.01; +58.6%, P <0.05). The NOS activity had significant positive correlation with the Vmax of high-affinity L-arginine transporter ( r =0.585, P <0.05). The changes of erythrocyte L-arginine transport were the same as that of kidney. The Vmax of SHR group was lower than that of WKY group (-30%, P <0.01), and the Vmax of CAP group was higher than that of SHR group (+26.5%, P <0.01). Km was not significantly changed. There is a positive correlation between the Vmax of L-arginine transport in erythrocyte and the Vmax of high- or low- affinity L-arginine transporter in renal tissue, ( r =0.8434, P <0.01, high-affinity; r =0.5255, P <0.05, low- affinity ). CONCLUSION: There existed a functional inhibition in L-arginine/nitric oxide pathway in the kidney of SHR. It can be recovered obviously by captopril treatment. The changes of L-arginine transport in kidney coincide with that in erythrocyte.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2000年第7期610-614,共5页
Chinese Journal of Pathophysiology
基金
广东省高教厅高校科技三项资助
