Elucidation of the molecular basis attributed to onset of abnormal retinal hemodynamics and strategy of novel prevention drugs for retinopathy

本研究表明，在糖尿病大鼠早期，通过大电导Ca^<2+>-激活的K^+(BK_<Ca>)通道激活介导的视网膜血管扩张反应减弱。此外，糖尿病大鼠视网膜血管氧化应激增加。因此，BK_<Ca>通道功能的损害和氧化应激的增加可能导致糖尿病视网膜血流动力学异常，从而在糖尿病视网膜病变的发病机制中起重要作用。总之，改善视网膜循环和具有抗氧化作用的药物被认为是预防视网膜病变的新候选药物。

This study demonstrated that retinal vasodilator responses mediated through the mechanism involving activation of the large-conductance Ca^<2+>-activated K^+(BK_<Ca>) channel was diminished at the early stage of diabetes in rats. Furthermore, it was suggested that the oxydative stress was increased in retinal blood vessels of diabetes rats. Thus, impairment of BK_<Ca> channel function and increased oxidative stress may contribute to abnormal retinal hemodynamics in diabetes and consequently play an important role in the pathogenesis of diabetic retinopathy. In conclusion, drugs that improve retinal circulation and possess antioxidative effect are considered to be novel candidates for prevention of retinopathy.