| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Outline of Final Research Achievements |
This study demonstrated that nitric oxide (NO)-induced vasodilator response is mediated via cycloocygenase/prostaglandin I2/prostanoid IP/cAMP signaling pathway and voltage-dependent potassium channel in rat retinal arterioles. Moreover, our results suggested that the activation of large-conductance calcium-activated potassium (BKCa) channels is involved in stimulation of beta2-adrenoceptor-mediated vasodilation of rat retinal arterioles. Increased oxidative stress may contribute to attenuate retinal vasodilator responses induced by an activator of BKCa channels in diabetic rats. Furthermore, the dysfunction of retinal arterioles in diabetic rats tended to be suppressed by administration of an antioxidant drug. In conclusion, drugs that improve retinal circulation and possess antioxidative effect are considered to be novel candidates for prevention of retinopathy.
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