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.
Keywords eNOS - vasodilation - EGCG - catechin - theaflavins - thearubigin
Returned for 1. Revision: 7 January 2008 1. Revision received: 3 July 2008 Returned for 2. Revision: 1 August 2008 2. Revision
received: 13 August 2008 Returned for 3. Revision: 26 September 2008 3. Revision received: 13 October 2008