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.