alexa Vasodilation As A Mechanism Of Cardio-protection Induced By Epicatechin | 72343
ISSN: 2167-0501

Biochemistry & Pharmacology: Open Access
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9th World Congress on Pharmacology

Aleksandra Novakovic, Marija Marinko, Goran Jankovic, Dragoslav Nenezic, Ivan Stojanovic, Predrag Milojevic, Vladimir Kanjuh, Qin
Yang, Guo-Wei He
University of Belgrade, Belgrade, Serbia
Institute for Cardiovascular Diseases “Dedinje”, Serbia
Academy of Sciences and Arts, Belgrade, Serbia
Chinese University of Hong Kong, Hong Kong
TEDA International Cardiovascular Hospital, China
Posters & Accepted Abstracts: Biochem Pharmacol (Los Angel)
DOI: 10.4172/2167-0501-C1-007
Abstract
Introduction: Epicatechin, along with catechin and procyanidins, belongs to flavanols, a major group of flavonoids in human diet. As many studies have demonstrated an inverse relationship between cardiovascular risk and consumption of flavanols, it has been suggested that epicatechin is likely a major bioactive constituent of flavanol-rich foods and beverages. One of its cardioprotective effect mechanisms is vasodilation. However, the exact mechanisms by which epicatechin causes vasodilation are unclear. Objectives: The present study aimed to investigate relaxant effect of epicatechin on the isolated human internal mammary artery (HIMA) and its underlying mechanisms. Methods: Discarded segments of HIMA were collected from patients undergoing coronary artery bypass grafting and studied in organ baths. Results: Epicatechin induced a concentration-dependent relaxation of HIMA rings pre-contracted by phenylephrine. Among the K+ channel blockers, 4-aminopyridine and margatoxin, blockers of voltage-gated K+ (KV) channels, and glibenclamide, a selective ATP-sensitive K+ (KATP) channels blocker, partly inhibited the epicatechin-induced relaxation of HIMA, while iberiotoxin, a most selective blocker of large conductance Ca2+-activated K+ channels (BKCa), almost completely inhibited the relaxation. In rings pre-contracted by 80 mM K+, epicatechin induced partial relaxation of HIMA, whereas in Ca2+-free medium, epicatechin completely relaxed HIMA rings pre-contracted by phenylephrine and caffeine. Finally, thapsigargin, a sarcoplasmic reticulum Ca2+-ATPase inhibitor, slightly antagonized epicatechin-induced relaxation of HIMA pre-contracted by phenylephrine. Conclusions: These results suggest that epicatechin induces strong endothelium-independent relaxation of HIMA precontracted by phenylephrine whilst 4-aminopyridine- and margatoxin-sensitive KV channels, as well as BKCa and KATP channels, located in vascular smooth muscle, mediate this relaxation. In addition, it seems that epicatechin could inhibit influx of extracellular Ca2+, interfere with intracellular Ca2+ release and re-uptake by the sarcoplasmic reticulum.
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