Involvement of endothelium/nitric oxide in vasorelaxation induced by purified green tea (−)epicatechin

Abstract

The present study investigated the involvement of endothelial nitric oxide in relaxation induced by purified green tea (−)epicatechin in rat isolated mesenteric arteries. (−)Epicatechin caused both endothelium-dependent and -independent relaxation. N G-Nitro- l-arginine methyl ester ( l-NAME, 100 μM) and methylene blue (10 μM) significantly attenuated (−)epicatechin-induced relaxation in endothelium-intact tissues. l-Arginine (1 mM) partially antagonized the effect of l-NAME. (−)Epicatechin-induced relaxation was inhibited by Rp-guanosine 3′,5′-cyclic monophosphothioate triethylamine. In contrast, indomethacin and glibenclamide had no effect. (−)Epicatechin (100 μM) significantly increased the tissue content of cyclic GMP and N G-nitro- l-arginine (100 μM) or removal of the endothelium abolished this increase. (−)Epicatechin (100 μM) induced an increase in intracellular Ca 2+ levels in cultured human umbilical vein endothelial cells. Iberiotoxin at 100 nM attenuated (−)epicatechin-induced relaxation in endothelium-intact arteries and this effect was absent in the presence of 100 μM l-NAME. In summary, (−)epicatechin-induced endothelium-dependent relaxation is primarily mediated by nitric oxide and partially through nitric oxide-dependent activation of iberiotoxin-sensitive K + channels. In addition, there may be a causal link between increased Ca 2+ levels and nitric oxide release in response to (−)epicatechin.