tryptophyl-histidine and Cardiovascular-Diseases

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.

Topics: Animals; Aorta; Cardiovascular Diseases; Catechin; Dipeptides; Drug Synergism; Humans; In Vitro Techniques; Male; Rats; Rats, Sprague-Dawley; Vasodilation; Vasodilator Agents