Mechanisms of the paradoxical effect of L-Arginine on glomerulosclerosis in 5/6 nephrectomized rats

它仍然存在影响，其中L-精氨酸（L-ARG）淀粉或aggravate renal功能和在renal疾病的几种模型中的历史学变化，而L-ARG是硝酸氧化物（NO）的基础合成酶，作为良好的前体和多胺的前体，其中由于renal纤维rosis。这些雄心勃勃的结果可能会归因于L-ARG管理员的剂量和周期的差异，以及在每个观察中使用的动物模型。因此，我们测试了L-ARG对平均血压（MBP）、蛋白质（UP）的24小时初级提取、无代谢物（NO I-D3-（/）2 I-D3 +NO I-D3-（/）3 I-D3）和环化GMP （cGMP）、等离子体不对称二甲基精氨酸（ADMA）、球状变黑指数（SI）和5/6碱性SD大鼠中的%国际纤维化区域（%INT）。5/6 nephrectomized SD rats were divided into 4 groups。1） L-ARG 0.2 g/kg/Day （0.2 gARG） 2） L-ARG 1 g/kg/Day （1 gARG） 3） L-ARG 2 g/kg/Day （2 gARG） 4） No admin\of L-ARG （ARG（-））。Compared with ARG（-） MBP， UP and ADMA were significantly decreased and NOイイD3-（/）2イエD3+NOイD3-（/）3イエD3， cGMP were significantly increased in 0.2 gARG。SI和%INT在2gARG中明显增加，在0.2gARG中减少。L-ARG淀粉淀粉样的小剂量和内纤维，而大剂量没有。SI，%INT and ADMA were inversely correlated with NO D3-（/）2-D3+NO-D3-（/）3-D3。这些数据提出了关于renal NO合成物可能会导致attenuate glomerulosclerosis和interstitial fibrosis，以及ADMA和L-ARG可能会导致decrease in NO。

It has been still controversial whether L-Arginine (L-ARG) ameliorate or aggravate renal function and histopathological changes in several models of renal disease, as L-ARG is the substrate for nitric oxide(NO) synthase as well as the precursor of proline and polyamines which cause renal fibrosis. These ambiguous results might be attributed to the difference in the dose and period of L-ARG administered, and animal model used in each observation. Therefore, we tested the dose-dependent effect of L-ARG on mean blood pressure (MBP), 24 hour urinary excretion of protein (UP), NO metabolites (NOィイD3-(/)2ィエD3+NOィイD3-(/)3ィエD3) and cyclic GMP (cGMP), plasma asymmetrical dimethylarginine (ADMA), glomerular sclerosis index (SI) and % interstitial fibrosis area (%INT) in 5/6 nephrectomized SD rats. 5/6 nephrectomized SD rats were divided into 4 groups. 1) L-ARG 0.2g/kg/day (0.2gARG) 2) L-ARG 1g/kg/day (1gARG) 3) L-ARG 2g/kg/day (2gARG) 4) No administration of L-ARG (ARG(-)). Compared with ARG(-) MBP, UP and ADMA were significantly decreased and NOィイD3-(/)2ィエD3+NOィイD3-(/)3ィエD3, cGMP were significantly increased in 0.2gARG. SI and %INT were significantly increased in 2gARG and decreased in 0.2gARG. Small dose of L-ARG ameliorated glomeruiosclerosis and interstitial fibrosis while larger dose did not. SI,%INT and ADMA were inversely correlated with NOィイD3-(/)2ィエD3+NOィイD3-(/)3ィエD3. These data suggested that renal NO synthesis might attenuate glomerulosclerosis and interstitial fibrosis and the rise in ADMA and L-ARG might cause the decrease in NO.