Biochemistry & Pharmacology: Open Access
Open Access
ISSN: 2167-0501
+44-20-4587-4809
ISSN: 2167-0501
+44-20-4587-4809
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)
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.