抄録
Flow-induced dilation has been widely observed in various arterioles. Increase of intraluminal flow is known to produce vasodilation of the arterioles via release of endogenous factors, such as NO, vasodilator prostanoids (PGs), and EDHF. In this study, we attempted to investigate the mechanisms of the flow-induced vasodilation in the pressurized rabbit cerebral penetrating arterioles. The arterioles (∼100 μm in diameter) were cannulated, and suffused with MOPS solution at 37°C. The inflow and outflow cannula was connected to different reservoirs which can be moved independently. The intraluminal flow was established by changing the height of inflow and outflow reservoirs with keeping the midpoint luminal pressure constant. After an equilibration period 40min, the pressurized arteriolar preparations developed spontaneous constricted to ∼50% of their maximal diameter. Intraluminal flow produced a dilation of the arterioles. L-NAME reduced the flow-induced vasodilation. Additional administration of the KCa channels inhibitor charybdotoxin and apamin further reduced the dilation. In the presence of L-NAME together with charybdotoxin and apamin, the residual vasodilation was completely diminished by additional treatment with indomethacin. The removal of endothelium completely abolished the flow-induced vasodilation of the arterioles. These findings suggest that in rabbit cerebral penetrating arterioles, the intraluminal flow produced flow-induced dilation via production and release of endogenous NO, PGs, and EDHF. [Jpn J Physiol 55 Suppl:S101 (2005)]
