(-)epicatechin induces and modulates endothelium-dependent relaxation in isolated rat mesenteric artery rings.
Abstract
AIM: The present study was aimed to examine the role of endothelial nitric oxide
in the relaxant response to green tea (-)epicatechin and its modulation of
endothelium-mediated relaxation in the isolated rat mesenteric artery rings.
METHODS: Changes in the isometric tension were measured with Grass
force-displacement transducers.
RESULTS: The (-)epicatechin-induced relaxation was largely dependent on the
presence of intact endothelium and was reversed by NG-nitro-L-arginine methyl
ester 10 micromol/L or methylene blue 10 micromol/L, the inhibitors of nitric
oxide-mediated relaxation. L-Arginine at 1 mmol/L antagonized the effect of
L-NAME or methylene blue. Pretreatment of endothelium-intact rings with
(-)epicatechin 10 micromol/L enhanced the relaxation induced by
endothelium-dependent vasodilator, acetylcholine, while this concentration did
not influence the endothelium-independent relaxation induced by sodium
nitroprusside in the endothelium-denuded artery rings.
CONCLUSION: The results indicate that the endothelium-dependent vasodilation by
(-)epicatechin is mainly mediated through nitric oxide and low concentration of
(-)epicatechin augments endothelium-dependent vasorelaxation in the rat
mesenteric arteries.
Keywords:
in the relaxant response to green tea (-)epicatechin and its modulation of
endothelium-mediated relaxation in the isolated rat mesenteric artery rings.
METHODS: Changes in the isometric tension were measured with Grass
force-displacement transducers.
RESULTS: The (-)epicatechin-induced relaxation was largely dependent on the
presence of intact endothelium and was reversed by NG-nitro-L-arginine methyl
ester 10 micromol/L or methylene blue 10 micromol/L, the inhibitors of nitric
oxide-mediated relaxation. L-Arginine at 1 mmol/L antagonized the effect of
L-NAME or methylene blue. Pretreatment of endothelium-intact rings with
(-)epicatechin 10 micromol/L enhanced the relaxation induced by
endothelium-dependent vasodilator, acetylcholine, while this concentration did
not influence the endothelium-independent relaxation induced by sodium
nitroprusside in the endothelium-denuded artery rings.
CONCLUSION: The results indicate that the endothelium-dependent vasodilation by
(-)epicatechin is mainly mediated through nitric oxide and low concentration of
(-)epicatechin augments endothelium-dependent vasorelaxation in the rat
mesenteric arteries.