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Endothelium‐dependent contraction of rat thoracic aorta induced by gallic acid
Author(s) -
Sanae Fujiko,
Miyaichi Yukinori,
Hayashi Hisao
Publication year - 2003
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.1255
Subject(s) - gallic acid , contraction (grammar) , endothelium , nitric oxide , phenylephrine , chemistry , sodium nitroprusside , pharmacology , biochemistry , medicine , endocrinology , antioxidant , organic chemistry , blood pressure
The vascular effect of a component of hydrolysable tannins, gallic acid, was examined in isolated rat thoracic aorta. Gallic acid exerted a contractile effect on the phenylephrine‐ or prostaglandin F 2/α ‐precontracted endothelium‐intact arteries. In endothelium‐denuded arteries, the contractile response togallic acid was absent. Pretreatment with N G ‐nitro‐ L ‐arginine methyl ester (30 μ M ) abolished the gallic acid‐induced contraction. Pretreatment with indomethacin (10 μ M ) or BQ610 (100 n M ) had no observed effect. Pretreatment with gallic acid (1–10 μ M ) significantly attenuated the relaxation induced by acetylcholine, and that with 10 μ M gallic acid also reduced the potency of sodium nitroprusside in the relaxation, without a reduction in efficacy, in endothelium‐denuded arteries. These findings indicate that gallic acid induced endothelium‐dependent contraction and strongly inhibited the endothelium‐dependent relaxation rather than the endothelium‐independent relaxation, probably through inhibition of endothelial nitric oxide (NO) production. Since NO plays an important role in vasodilative regulation and inflammatory disorders, these findings may also indicate that gallic acid interferes with the inflammatory responses. Copyright © 2003 John Wiley & Sons, Ltd.