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Tsuneaki Omae, Taiji Nagaoka, Ichiro Tanano, Shinichi Otani, Takayuki Kamiya, Akitoshi Yoshida, III; Fenofibrate Elicits Dilation Of Isolated Porcine Arterioles. Invest. Ophthalmol. Vis. Sci. 2011;52(14):6050.
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Fenofibrate has been shown to have anti-inflammatory and atheroprotective effects on vascular tissue. Clinical study has demonstrated that fenofibrate is effective for diabetic retinopathy. However, the mechanism for the ocular vascular benefit of fenofibrate is still unclear and its action in the retinal microcirculation remains unknown. In the current study, we examined the direct effect and underlying mechanism of the vasomotor action of fenofibrate in porcine retinal arterioles.
Porcine retinal arterioles (60-90 µm in internal diameter) were isolated, cannulated and pressurized (55 cmH2O) without flow for in vitro study. Videomicroscopic techniques were employed to record diameter change in response to fenofibrate.
Retinal arterioles dilated dose-dependently in response to fenofibrate (10 n-30 µM). This vasodilation was significantly reduced after removal of the endothelium (p<0.0001). The nitric oxide (NO) synthase inhibitor N-nitro-L-arginine methyl ester, L-NAME (10 µM), exhibited an inhibitory effect on fenofibrate-induced vasodilation comparable to that produced by the denudation (p<0.0001). Pretreatment of compound C, AMP activated protein kinase inihibitor (10 µM), significantly reduced the vasodilation in same manner as that of L-NAME (p<0.0001).
Fenofibrate elicits mainly endothelium-dependent dilation of retinal arterioles. The present findings suggest that fenofibrate-induced vasodilation is mediated by the released NO via AMP activated protein kinase activation in retinal vascular endothelial cells.
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