title: Green and black tea are equally potent stimuli of NO production and vasodilation: new insights into tea ingredients involved.
abstract: Epidemiological studies suggest that consumption of tea is associated with beneficial cardiovascular effects. Since different types of tea are consumed throughout the world, a question of much interest is whether green tea is superior to black tea in terms of cardiovascular protection. We therefore compared the effects of green and black tea on nitric oxide (NO) production and vasodilation and elucidated the tea compounds involved. We chose a highly fermented black tea and determined concentrations of individual tea compounds in both green and black tea of the same type (Assam). The fermented black tea was almost devoid of catechins. However, both teas stimulated eNOS activity and phosphorylation in bovine aortic endothelial cells (BAEC) as well as vasorelaxation in rat aortic rings to a similar extent. In green tea, only epigallocatechin-3-gallate (EGCG) resulted in pronounced NO production and NO-dependent vasorelaxation in aortic rings. During tea processing to produce black tea, the catechins are converted to theaflavins and thearubigins. Individual black tea theaflavins showed a higher potency than EGCG in NO production and vasorelaxation. The thearubigins in black tea are highly efficient stimulators of vasodilation and NO production. Green and black tea compounds induced comparable phosphorylation of eNOS and upstream signalling kinases. Whereas stimulation of eNOS activity by EGCG was only slightly affected by pretreatment of cells with various ROS scavengers, TF3(theaflavin-3',3-digallate)-induced eNOS activity was partially inhibited by PEG-catalase. These results implicate that highly fermented black tea is equally potent as green tea in promoting beneficial endothelial effects. Theaflavins and thearubigins predominantly counterbalance the lack of catechins in black tea. The findings may underline the contribution of black tea consumption in prevention of cardiovascular diseases.
authors.affiliation: Medizinische Klinik mit Schwerpunkt Kardiologie und Angiologie Charité, Universitätsmedizin Berlin, CCM, Charitéplatz 1, Berlin, Germany.
authors.forename: Mario
authors.initials: M
authors.lastname: Lorenz
authors.forename: Janka
authors.initials: J
authors.lastname: Urban
authors.forename: Ulrich
authors.initials: U
authors.lastname: Engelhardt
authors.forename: Gert
authors.initials: G
authors.lastname: Baumann
authors.forename: Karl
authors.initials: K
authors.lastname: Stangl
authors.forename: Verena
authors.initials: V
authors.lastname: Stangl
mesh_terms: D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000502:physiology; D001628:Beverages / Q000706:statistics & numerical data*; D001921:Brain; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D002417:Cattle; D004730:Endothelium, Vascular / Q000187:drug effects / Q000201:enzymology / Q000502:physiology*; D006801:Humans; D006854:Hydrocortisone / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D052250:Nitric Oxide Synthase Type III / Q000187:drug effects / Q000378:metabolism; D013662:Tea; D014020:Tissue Extracts / Q000494:pharmacology; D014664:Vasodilation / Q000502:physiology*
chemical_list: D013662:Tea; D014020:Tissue Extracts; D009569:Nitric Oxide; D002392:Catechin; C045651:epigallocatechin gallate; D052250:Nitric Oxide Synthase Type III; D006854:Hydrocortisone