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R. H. Rosa, Jr., T. W. Hein, H. Liu, W. Xu, L. Kuo; Role of the Endothelium in Retinal Arteriolar Dilation to Increased Lumenal Flow. Invest. Ophthalmol. Vis. Sci. 2009;50(13):395.
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Flow-sensitive vasomotor responses play a critical role in the control of local blood flow in many organ systems. We previously established the existence of flow-induced responses in isolated retinal arterioles; however, the role of the endothelium and the associated cell signaling mechanisms in these vasomotor responses have not been systematically characterized. Herein, we employed an isolated vessel approach to specifically address these issues.
Second-order porcine retinal arterioles were isolated, cannulated, and pressurized to 55 cmH2O lumenal pressure by two independent reservoir systems. The lumenal flow was increased stepwise by creating hydrostatic pressure gradients across two reservoirs. Diameter changes were recorded using videomicroscopic techniques. The role of the endothelium in flow-induced dilation was assessed by intraluminal perfusion of the nonionic detergent CHAPS (0.4%) to remove endothelial cells. Disruption of the endothelium was verified by the absence of vasodilation in response to the endothelium-dependent vasodilator bradykinin (10 nM) while maintaining normal dilation to the smooth muscle relaxing agent sodium nitroprusside (10 nM to 10 µM). The roles of endothelium-derived prostaglandins and nitric oxide (NO) in the flow-induced response were investigated by treating the vessels with their synthesis inhibitors indomethacin (10 µM) and L-NAME (10 µM), respectively.
Retinal arterioles developed basal tone (64±7 µm) under zero flow conditions. A stepwise increase in lumenal flow produced a graded dilation of retinal arterioles. Endothelial denudation with CHAPS abolished flow-induced vasodilation. Indomethacin did not alter the flow-induced vasodilatory response, whereas L-NAME abolished this response.
Flow-induced vasodilation occurs in porcine retinal arterioles and is mediated by the endothelium via activation of NO synthase. Prostaglandin synthesis does not appear to play a role in flow-induced dilation of retinal arterioles. Additional studies are necessary to further elucidate the cell signaling mechanisms responsible for this important vasomotor response.
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