The aim of the present study was to clarify the participation of endogenous arachidonic acid (AA) metabolites in regulating porcine basilar, coronary, pulmonary and mesenteric arterial tones in vitro. A cyclooxygenase inhibitor, indomethacin, relaxed basilar artery but not other arteries examined. Quinacrine (a phospholipase A2 inhibitor), OKY-046 (a thromboxane (TX) A2 synthetase inhibitor) and ONO-3708 (a TXA2/prostaglandin H2 receptor antagonist) produced relaxation in basilar arteries with intact endothelium. Nordihydroguaiaretic acid (a lipoxygenase inhibitor) had no effect on the tone. The amount of TXB2 (a stable metabolite of TXA2) spontaneously released from porcine basilar arteries was 6-10 fold more than those from other arteries. Indomethacin and OKY-046 mostly inhibited the production of TXB2. Endothelial denudation decreased indomethacin-induced relaxation and the amount of TXB2. These results suggest that a vasoconstricting substance(s) is released from endothelial cells and possibly smooth muscle cells in porcine basilar arteries in vitro. The main constricting substance is proposed to be TXA2. On the other hand, several arteries from peripheral vascular beds did not release this vasoconstricting substance.