Altered endothelium-dependent responsiveness in the aortas and renal arteries of Otsuka Long–Evans Tokushima Fatty (OLETF) rats, a model of non-insulin-dependent diabetes mellitus

Satomi Kagota, Yu Yamaguchi, Kazuki Nakamura, Masaru Kunitomo
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引用次数: 53

Abstract

We examined endothelium-dependent relaxation in the aortas and renal arteries of Otsuka Long–Evans Tokushima Fatty (OLETF) rats, a model of non-insulin-dependent diabetes mellitus, in comparison with non-diabetic Long–Evans Tokushima Otsuka rats as controls. Acetylcholine-induced relaxation in both arteries was attenuated, and the attenuation was restored to the control level by indomethacin. The relaxation was inhibited completely in the aortas, but only partially in renal arteries by NG-nitro-l-arginine methyl ester, and the degree of the latter inhibition was greater in OLETF rats than in the controls. The relaxation was inhibited by aminoguanidine in both arteries of OLETF rats but not in the controls. Serum NO2 plus NO3 levels significantly increased in OLETF rats. These results suggest that impairment of relaxation in OLETF rat arteries is due to increased release of contractile factors but not decreased release of nitric oxide.

非胰岛素依赖型糖尿病大鼠(OLETF)主动脉和肾动脉内皮依赖性反应性的改变
我们检测了非胰岛素依赖型糖尿病大鼠(OLETF)主动脉和肾动脉内皮依赖性松弛,并与非糖尿病大鼠(Long-Evans Tokushima Otsuka)作为对照。乙酰胆碱引起的双动脉舒张减弱,吲哚美辛可使其恢复到对照水平。ng -硝基精氨酸甲酯可完全抑制主动脉舒张,而肾动脉舒张仅部分抑制,且OLETF大鼠对肾动脉舒张的抑制程度大于对照组。胺胍对OLETF大鼠双动脉舒张有抑制作用,而对对照组无抑制作用。OLETF大鼠血清NO2和NO3水平显著升高。这些结果表明,OLETF大鼠动脉舒张损伤是由于收缩因子释放增加而不是一氧化氮释放减少。
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