Green Tea Ingestion Greatly Reduces Plasma Concentrations of Nadolol in Healthy Subjects. Issue 4 (13th January 2014)

• Record Type: Journal Article
• Authors: Misaka, S; Yatabe, J; Müller, F; Takano, K; Kawabe, K; Glaeser, H; Yatabe, M S; Onoue, S; Werba, J P; Watanabe, H; Yamada, S; Fromm, M F; Kimura, J
• Is Part Of: Clinical pharmacology & therapeutics. Volume 95:Issue 4(2014)
• Page Start: 432
• Page End: 438
• Publication Date: 2014-01-13
• Subjects: Pharmacology -- Periodicals; Therapeutics -- Periodicals; 615.5
• DOI: 10.1038/clpt.2013.241
• Languages: English
• ISSNs: 0009-9236

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <p>This study aimed to evaluate the effects of green tea on the pharmacokinetics and pharmacodynamics of the <italic>β</italic>‐blocker nadolol. Ten healthy volunteers received a single oral dose of 30 mg nadolol with green tea or water after repeated consumption of green tea (700 ml/day) or water for 14 days. Catechin concentrations in green tea and plasma were determined. Green tea markedly decreased the maximum plasma concentration (<italic>C</italic><sub>max</sub>) and area under the plasma concentration–time curve (AUC<sub>0–48</sub>) of nadolol by 85.3% and 85.0%, respectively (<italic>P</italic> < 0.01), without altering renal clearance of nadolol. The effects of nadolol on systolic blood pressure were significantly reduced by green tea. [<sup>3</sup>H]‐Nadolol uptake assays in human embryonic kidney 293 cells stably expressing the organic anion–transporting polypeptides OATP1A2 and OATP2B1 revealed that nadolol is a substrate of OATP1A2 (Michaelis constant (<italic>K</italic><sub>m</sub>) = 84.3 μmol/l) but not of OATP2B1. Moreover, green tea significantly inhibited OATP1A2‐mediated nadolol uptake (half‐maximal inhibitory concentration, <italic>IC</italic><sub>50</sub> = 1.36%). These results suggest that green tea reduces plasma concentrations of nadolol possibly in part by inhibition of OATP1A2‐mediated uptake of nadolol in the intestine.</p> <p> <italic>Clinical Pharmacology & Therapeutics</italic> (2014); <bold>95</bold> 4, 432–438. doi:<ext-link ext-link-type="doi" xlink:type="simple" xmlns:xlink="http://www.w3.org/1999/xlink">10.1038/clpt.2013.241</ext-link></p> </abstract>