Epigallocatechin gallate promotes the vasorelaxation power of the antiatherosclerotic dipeptide Trp-His in contracted rat aorta.
The aim of this study was to demonstrate the enhancement of the vasorelaxation power of the antiatherosclerotic voltage-dependent L-type Ca(2+) channel (VDCC)-blocking peptide Trp-His by epigallocatechin gallate (EGCg). We found that 300 μM EGCg dramatically enhanced the magnitude of Trp-His-induced vasorelaxation by a factor of >6 (EC(50) of Trp-His: EGCg(-), 2.80 ± 0.05 mM; EGCg(+), 0.45 ± 0.04 mM) in phenylephrine-contracted rat aorta. The enhancing effect of EGCg was completely abolished in endothelium-removed aorta and high K(+)-contracted aorta. The enhancement of Trp-His-induced vasorelaxation by EGCg was significantly diminished by either N(G)-monomethyl-l-arginine acetate (NO synthase (NOS) inhibitor) or 1-H-[1,2,4]oxadiazolo[4,3]quinoxalin-1-one (soluble guanylyl cyclase inhibitor), together with the enhancement of NOS activity by EGCg. These results indicate that the enhancing effect of EGCg in Trp-His-induced vasorelaxation may be involved in the activation of NO/cGMP pathway.
Graduate School of Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka 812-8581, Japan. mitsurut@agr.kyushu-u.ac.jp
Mitsuru
M
Tanaka
Jian
J
Zhao
Aki
A
Suyama
Toshiro
T
Matsui
D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000188:drug therapy / Q000503:physiopathology; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D004151:Dipeptides / Q000494:pharmacology*; D004357:Drug Synergism; D006801:Humans; D066298:In Vitro Techniques; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology*
D004151:Dipeptides; D014665:Vasodilator Agents; C509582:tryptophyl-histidine; D002392:Catechin; C045651:epigallocatechin gallate