Okadaic acid (OA) isolated from black sponge (Halichondria) caused tonic contractions of human umbilical arteries and rabbit aorta both in the presence and absence of Ca2+. This tonic contraction was not affected by Ca2+ chelator, Ca2+ entry blockers and La3+. In addition, the antagonists of alpha-adrenoceptors, histamine, serotonin and ACh receptors had no effect on the OA-induced contraction. High K, ouabain and indomethacin failed to inhibit the response to OA. However, the combination of anaerobic conditions and absence of glucose abolished the response to OA. OA had no effect on the myosin B ATPase and saponin-treated skinned fibers of rabbit aorta. The contractile action of OA may not also be related to calmodulin-related PDE and mitochondrial respiration. In conclusion, although the precise mode of action is not evident at the present time, OA, in its unique pharmacological action – that of producing sustained contraction independent of extracellular Ca2+ -may alter the handling of Ca2+ to intracellular store sites.