The effects of the active principles of crude ginger (a traditional Sino-Japanese medicine), the gingerols, on the contractile responses to eicosanoids were compared using isolated mouse and rat blood vessels. Leukotrienes (LT) C₄ and D₄, a thromboxane (TX) A₂ derivative (U-46619), prostaglandins (PG) F_2α, PG1₂-Na, PGE₂, the stable PGI₂ derivative TRK-100, and PGD₂ induced contraction in longitudinal segments of mouse mesenteric veins in that order of potency. Exogenous arachidonic acid and PGE₁, did not cause contraction. The mesenteric veins also contracted in response to noradrenaline (NA) and phenylephrine (PhE), but not to clonidine. The gingerols alone relaxed the muscle transiently and then augmented the response to PGF_2α, PGE₂, PGI₂-Na, and TRK-100, but suppressed the response to PGD₂, U-46619, LTC₄, LTD₄, NA and PhE. (±)-[6]-Gingerol also potentiated the PGF_2α-induced contraction in longitudinal segments of rat mesenteric vein and vena cava, but inhibited it in circular segments of rat aorta and longitudinal segments of mouse mesenteric arteries. These results showed that (±)-[6]- and (±)-[8]-gingerols potentiated the contraction induced by prostanoids (except PGD₂) and inhibited that produced by PGD₂, TXA₂, and LT, suggesting the modulation of eicosanoids-induced responses by (±)-[6]- or (±)-[8]-gingerol.