Effects of green tea, black tea and Rooibos tea on angiotensin-converting enzyme and nitric oxide in healthy volunteers. 2010

Ingrid A-L Persson, and Karin Persson, and Staffan Hägg, and Rolf G G Andersson
Department of Medical and Health Sciences, Division of Drug Research/Pharmacology, Faculty of Health Sciences, Linköping University, SE-581 85 Linköping, Sweden. ingrid.persson@liu.se

OBJECTIVE Tea has been reported to reduce cardiovascular mortality, but the underlying mechanisms are largely unknown. The aim of the current project was to investigate the effect of green tea (Japanese Sencha), black tea (Indian Assam B.O.P.) and Rooibos tea (South Africa) on angiotensin-converting enzyme (ACE) and nitric oxide (NO). METHODS Seventeen healthy volunteers received a single oral dose of 400 ml green tea, black tea or Rooibos tea in a randomized, three-phase, crossover study. ACE activity and NO concentration were measured (at 0, 30, 60 and 180 min) in all phases. ACE activity was analysed by means of a commercial radioenzymatic assay. Nitrite was analysed as a marker of NO concentration. In addition, ACE genotype was determined using a PCR method. RESULTS Oral intake of a single dose of Rooibos tea significantly inhibited ACE activity after 30 min (P < 0.01) and after 60 min (P < 0.05). A significant inhibition of ACE activity was seen with green tea for the ACE II genotype 30 min after intake of the tea (P < 0.05) and for the ACE ID genotype 60 min after intake (P < 0.05). A significant inhibition of ACE activity was also seen with Rooibos tea for the ACE II genotype 60 min after intake (P < 0.05). No significant effect on NO concentration was seen. CONCLUSIONS These results suggest that green tea and Rooibos tea may have cardiovascular effects through inhibition of ACE activity.

UI MeSH Term Description Entries
D007703 Peptidyl-Dipeptidase A A peptidyl-dipeptidase that catalyzes the release of a C-terminal dipeptide, oligopeptide-|-Xaa-Yaa, when Xaa is not Pro, and Yaa is neither Asp nor Glu. Thus, conversion of ANGIOTENSIN I to ANGIOTENSIN II, with increase in vasoconstrictor activity, but no action on angiotensin II. It is also able to inactivate BRADYKININ, a potent vasodilator; and has a glycosidase activity which releases GPI-anchored proteins from the membrane by cleaving the mannose linkage in the GPI moiety. (From https://www.uniprot.org April 15, 2020). ACE1 Angiotensin-Converting Enzyme 1,ACE1 Protein,Angiotensin Converting Enzyme,Angiotensin Converting Enzyme 1,Antigens, CD143,CD143 Antigens,Dipeptidyl Carboxypeptidase I,Kininase II,Peptidase P,Angiotensin I-Converting Enzyme,Carboxycathepsin,Dipeptidyl Peptidase A,Kininase A,ACE1 Angiotensin Converting Enzyme 1,Angiotensin I Converting Enzyme,Carboxypeptidase I, Dipeptidyl,Peptidyl Dipeptidase A
D008297 Male Males
D009569 Nitric Oxide A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP. Endogenous Nitrate Vasodilator,Mononitrogen Monoxide,Nitric Oxide, Endothelium-Derived,Nitrogen Monoxide,Endothelium-Derived Nitric Oxide,Monoxide, Mononitrogen,Monoxide, Nitrogen,Nitrate Vasodilator, Endogenous,Nitric Oxide, Endothelium Derived,Oxide, Nitric,Vasodilator, Endogenous Nitrate
D005260 Female Females
D005838 Genotype The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS. Genogroup,Genogroups,Genotypes
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000328 Adult A person having attained full growth or maturity. Adults are of 19 through 44 years of age. For a person between 19 and 24 years of age, YOUNG ADULT is available. Adults
D000806 Angiotensin-Converting Enzyme Inhibitors A class of drugs whose main indications are the treatment of hypertension and heart failure. They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility. ACE Inhibitor,ACE Inhibitors,Angiotensin Converting Enzyme Inhibitor,Angiotensin I-Converting Enzyme Inhibitor,Angiotensin-Converting Enzyme Inhibitor,Kininase II Inhibitor,Kininase II Inhibitors,Angiotensin I-Converting Enzyme Inhibitors,Angiotensin-Converting Enzyme Antagonists,Antagonists, Angiotensin-Converting Enzyme,Antagonists, Kininase II,Inhibitors, ACE,Inhibitors, Angiotensin-Converting Enzyme,Inhibitors, Kininase II,Kininase II Antagonists,Angiotensin Converting Enzyme Antagonists,Angiotensin Converting Enzyme Inhibitors,Angiotensin I Converting Enzyme Inhibitor,Angiotensin I Converting Enzyme Inhibitors,Antagonists, Angiotensin Converting Enzyme,Enzyme Antagonists, Angiotensin-Converting,Enzyme Inhibitor, Angiotensin-Converting,Enzyme Inhibitors, Angiotensin-Converting,II Inhibitor, Kininase,Inhibitor, ACE,Inhibitor, Angiotensin-Converting Enzyme,Inhibitor, Kininase II,Inhibitors, Angiotensin Converting Enzyme
D001628 Beverages Liquids that are suitable for drinking. (From Merriam Webster Collegiate Dictionary, 10th ed) Beverage
D013662 Tea The infusion of leaves of CAMELLIA SINENSIS (formerly Thea sinensis) as a beverage, the familiar Asian tea, which contains CATECHIN (especially epigallocatechin gallate) and CAFFEINE. Black Tea,Green Tea,Black Teas,Green Teas,Tea, Black,Tea, Green,Teas, Black,Teas, Green

Related Publications

Ingrid A-L Persson, and Karin Persson, and Staffan Hägg, and Rolf G G Andersson
February 2016, Food & function,
Ingrid A-L Persson, and Karin Persson, and Staffan Hägg, and Rolf G G Andersson
May 1998, British journal of pharmacology,
Ingrid A-L Persson, and Karin Persson, and Staffan Hägg, and Rolf G G Andersson
October 1992, British journal of clinical pharmacology,
Ingrid A-L Persson, and Karin Persson, and Staffan Hägg, and Rolf G G Andersson
September 1992, British journal of clinical pharmacology,
Ingrid A-L Persson, and Karin Persson, and Staffan Hägg, and Rolf G G Andersson
July 2021, Journal of Zhejiang University. Science. B,
Ingrid A-L Persson, and Karin Persson, and Staffan Hägg, and Rolf G G Andersson
June 2020, European journal of drug metabolism and pharmacokinetics,
Ingrid A-L Persson, and Karin Persson, and Staffan Hägg, and Rolf G G Andersson
September 1993, Journal of cardiovascular pharmacology,
Ingrid A-L Persson, and Karin Persson, and Staffan Hägg, and Rolf G G Andersson
June 1993, Circulation research,
Ingrid A-L Persson, and Karin Persson, and Staffan Hägg, and Rolf G G Andersson
January 2010, Journal of immunoassay & immunochemistry,
Ingrid A-L Persson, and Karin Persson, and Staffan Hägg, and Rolf G G Andersson
October 1991, European journal of clinical investigation,
Copied contents to your clipboard!