Abstract
Cat cortical arterioles and venules were exposed in vivo to the Ca2+ antagonist nifedipine under normal conditions and in focal ischemia. Topical application of nifedipine caused a marked, concentration-dependent arteriolar dilatation. The dilatatory responses increased significantly with decreasing arteriolar size. Perivenular microapplication of nifedipine invariably caused dilatation that was less pronounced but more long-lasting than that on the arteriolar side. Arterioles, which constricted after middle cerebral artery occlusion, invariably dilated following nifedipine application. These dilatatory responses were transient but could be repeated, and on some occasions were accompanied by a return of flow in vessels in which stasis had been present. The results suggest that nifedipine is able to dilate cerebral vessels both under normal conditions and when contracted during focal ischemia.