Endothelial NO Production Is Mandatory for Epigallocatechin-3-Gallate–induced Vasodilation: Results From eNOS Knockout (eNOS(−/−)) Mice

The underlying mechanisms for the vasodilating effects of the tea catechin epigallocatechin-3-gallate (EGCG) are still not fully understood. Besides nitric oxide (NO)-dependent effects, other modes of action are discussed. To elucidate whether the NO pathway is a prerequisite in mediating vasodilating effects, we investigated EGCG-induced vasorelaxation in isolated aortic rings of endothelial nitric oxide knockout (eNOS(−/−)) mice. Vasodilation to acetylcholine was fully prevented in aortic rings of eNOS(−/−) mice, confirming lack of vascular NO production. Vasodilation to the exogenous NO donor sodium nitroprusside was preserved in eNOS(−/−) mice aortic rings. Low concentrations of EGCG (5–15 µM) resulted in strong vasorelaxation in aortic rings of wild type mice, whereas it was completely absent in eNOS(−/−) mice. In corroboration, relaxation in response to green tea was significantly inhibited in aortic rings of eNOS(−/−) mice. These results demonstrate that EGCG-induced vasodilation strongly relies on functional NO synthase in endothelial cells and subsequent stimulation of NO production in vessels.