Impaired Nitric Oxide-Mediated Vasodilation in Patients with Autosomal Dominant Polycystic Kidney Disease

摘要

We hypothesized that nitric oxide (NO) system is involved in the development of cardiovascular changes in autosomal dominant polycystic kidney disease (ADPKD). Small subcutaneous resistance vessels from prediaiysis ADPKD patients (n=7) and normal controls (n=9) were mounted in a Mulvany-Halpem myograph. The endothelium-dependent relaxation before and after vessel incubated with L-arginine (a substrate of NO synthase) or N~G nitro-Larginine methyl ester (L-NAME, an inhibitor of NO synthase), as well as endothelium-independent relaxation were investigated. The results showed: 1) The max relaxation rate of endothelium-dependent relaxation induced by acetylcholine (ACh) was 64,35+-21,70 vs. 87,57+-6,11(ADPKD vs. control, P<0.05); 2) In the presence of L-arginine, a left-shift of the ACh dose response curves was increased in normals, but not in ADPKD patients. The relaxation rate induced by high concentration of ACh (> 1 0-7 mol/1) were higher in controls than in ADPKD (P<0.05); 3). In the presence of the L-NAME the right-shift of the ACh dose-response curve was slighter in ADPKD man in controls (P<0.05); 4). The max relaxation rate of endothelium-independent relaxation mediated by 3-morphollino-sydnonimine (NO donor) was similar in the two groups.