Potentiation of vasoconstrictor response and inhibition of endothelium-dependent vasorelaxation by gallic acid in rat aorta.

In the isolated rat thoracic aorta, gallic acid potentiated the vasoconstrictor response to phenylephrine. The potentiation produced by gallic acid was absent in endothelium-denuded arteries. The potentiation was abolished by N(G)-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthesis, and slightly attenuated by an addition of L-arginine, while indomethacin or BQ610 had no effect. The potentiation of response to phenylephrine was not found for structural modifications of gallic acid, except for caffeic acid. Gallic acid also inhibited vasorelaxation induced by acetylcholine, sodium nitroprusside or prostacyclin, especially that by acetylcholine. The effect on vasorelaxation induced by acetylcholine was decreased by esterification of the carboxy group of gallic acid, and in the absence or by the methylation of the o-dihydroxy group. Caffeic acid inhibited the vasorelaxation, though the effect was smaller than that of gallic acid. These findings indicate that gallic acid produces a potentiation of contractile response and inhibition of vasorelaxant responses, probably through inactivation of nitric oxide (NO), in which endothelially produced NO is principally involved, and that the modification of functional groups of the gallic acid molecule abolishes the potentiation of contractile response and attenuates the inhibition of vasorelaxant responses.