Flow-mediated dilatation has been described mainly in peripheral conduit arteries. The goal of this study was to examine mechanisms and functional implications of flow-mediated dilatation in large cerebral arteries in vivo. Vessel diameter and velocity of blood flow through the basilar artery were measured using a cranial window in 45 anesthetized rats. Mean blood flow velocity through the basilar artery increased by 94 +/- 8% during unilateral common carotid artery occlusion and 203 +/- 13% during bilateral occlusion. Diameter of the basilar artery increased by 10 +/- 1% during unilateral common carotid artery occlusion and 29 +/- 2% during bilateral occlusion from control diameter of 275 +/- 8-mu-m. Vasodilatation appeared with a delay of 13 +/- 1 seconds after the onset of the increase in How velocity. With systemic arterial pressure maintained at baseline levels, pressure in the basilar artery (servonull) decreased initially during carotid occlusion, and during dilatation of the basilar artery, pressure was restored partially toward normal. Indomethacin (10 mg/kg i.v.), topical application of tetrodotoxin (10(-6) M), N(G)-monomethyl L-arginine (5 x 10(-6) M), tetraethylammonium chloride (10(-2) M), glibenclamide (10(-5) M), SKF 525A (3 x 10(-5) M), and ouabain (10(-5) M) had no effect on flow-mediated dilatation. These findings indicate that 1) pronounced dilatation of the basilar artery occurs in response to an increase in blood flow in vivo, 2) dilatation of large arteries attenuates reductions in cerebral microvascular pressure during increases in blood flow, and 3) flow-mediated dilatation of the basilar artery does not appear to depend solely on cyclooxygenase activity, formation of nitric oxide, voltage-dependent or ATP-sensitive K+ channels, activity of cytochrome P-450-dependent monooxygenase, or sodium pump activity.
