Endothelium-Dependent Potentiation of Prostaglandin F2.ALPHA.-Induced Contractions by (.+-.)-[6]-Gingerol Is Inhibited by Cyclooxygenase- but Not Lipoxygenase-Inhibitors in Mouse Mesenteric Veins.

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  • Endothelium-Dependent Potentiation of Prostaglandin F2α-Induced Contractions by(±)-[6]-Gingerol Is Inhibited by Cyclooxygenase-but Not Lipoxygenase-Inhibitors in Mouse Mesenteric Veins
  • Endothelium-Dependent Potentiation of P

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The mechanism of potentiation of prostaglandin (PG) F2α-induced contraction of mouse mesenteric veins by (±)-[6]-gingerol was investigated in vitro. (±)-[6]-Gingerol (0.3 mM) potentiated the maximal contraction response elicited by PGF2α (0.28 mM) in the presence of intact vascular endothelium, but not in its absence (de-endothelialized preparations). The potentiating effect was completely inhibited by cyclooxygenase inhibitors (0.2 mM aspirin and 0.2 mM indomethacin) and partly by calcium antagonists (2 μM verapamil, 8 nM nitrendipine and 1 μM ryanodine), but not inhibited by nordihydroguaiaretic acid (NDGA), a lipoxygenase inhibitor and ONO-3708, a thromboxane (TX) A2 antagonist. The potentiation by (±)-[6]-gingerol is also observed in mesenteric veins of streptozotocin-diabetic mice where the enhancement of PGF2α-induced contraction is caused mainly by activation of lipoxygenase. The potentiaion of PGF2α-induced contraction by (±)-[6]-gingerol may be caused by a cyclooxygenase-dependent release of vasoconstrictors, other than PGF2α and TXA2, or by inhibiting vasorelaxants released from endothelial cells of mouse mesenteric veins.

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