Endothelium-dependent contractions to arachidonic acid are mediated by products of cyclooxygenase.

Abstract

Arachidonic acid produces endothelium-dependent relaxation in canine arteries and endothelium-dependent contraction in veins. In canine femoral arteries, the relaxation is prevented by inhibitors of cyclooxygenase. To determine the role of cyclooxygenase in the contraction evoked by arachidonic acid in the veins, rings of canine femoral and intrapulmonary veins, with and without endothelium, were suspended in organ chambers and set at their optimum length for isometric tension measurements. In rings of femoral and pulmonary vein contracted with norepinephrine, arachidonic acid produced a concentration-dependent increase in tension that was eliminated by removal of the endothelium or by treatment with the inhibitors of cyclooxygenase (indomethacin, meclofenamate, or acetylsalicyclic acid). The contractions were not prevented by inhibitors of thromboxane synthetase or prostacyclin synthetase or lipoxygenase. Pulmonary and femoral veins with or without endothelium relaxed to low, but contracted to high concentrations of prostacyclin and prostaglandin E2. Prostaglandin F2 alpha caused endothelium-independent contractions in both blood vessels. The present study suggests that the endothelium-dependent contractions to arachidonic acid observed in canine veins are mediated by prostanoids other than thromboxane and prostacyclin.