Vanadate is a trace element in animal tissues and has been known to inhibit NA(+)-K(+) ATPase in various tissues including skeletal and cardiac muscles and smooth muscles. Vanadate shows contractile actions on various types of smooth muscles. Prolonged dietary administration of vanadate has been shown to cause arterial hypertension, increased peripheral resistance, and a marked reduction of coronary, visceral and renal blood flow.In isolated vascular smooth muscle of aorta, application of vanadate caused contraction. These studies have been conducted the preparation of vascular smooth muscles from which endothelial cell were removed. It has been reported that endothelial cell releases relaxing factor(s) (endothelium-derived relaxing factor, EDRF) in response to acetylcholine and a number of other stimuli and also produces vasoconstrictor substances (endothelium-derived contracting factor, EDCF). The aim of this present experiment is to elucidate whether vascular response of isolated rabbit aorta induced by vanadate are endothelium dependent or not. The result obtained were summarized as follows ; 1) When endothelium was intact, vanadate induced vascular relaxation of aorta precontracted with norepinephrine. But K+ induced contraction was augmented by vanadate in the aorta with or without endothelium. Whereas relaxation produced by vanadate precontracted with angiotensin II was endothelium-independent. 2) Hemoglobin, methylene blue, hydroquinone, and verapamil inhibited vanadate-induced vascular relaxation. But indomethacin and quinacrine had no effect on vanadate induced vascular relaxation. From the above results, it is speculated the vanadate act on endothelium, modifies the synthesis or release of endothelium-dependent relaxing factor and thus changes the contractile responses to norepinephrine in rabbit aorta.