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) C
4 and D
4, a thromboxane (TX) A
2 derivative (U-46619), prostaglandins (PG) F
2α, PG1
2-Na, PGE
2, the stable PGI
2 derivative TRK-100, and PGD
2 induced contraction in longitudinal segments of mouse mesenteric veins in that order of potency. Exogenous arachidonic acid and PGE
1, 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, PGE
2, PGI
2-Na, and TRK-100, but suppressed the response to PGD
2, U-46619, LTC
4, LTD
4, 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 PGD
2) and inhibited that produced by PGD
2, TXA
2, and LT, suggesting the modulation of eicosanoids-induced responses by (±)-[6]- or (±)-[8]-gingerol.
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