E. Andriambeloson et al., Mechanism of endothelial nitric oxide-dependent vasorelaxation induced by wine polyphenols in rat thoracic aorta, J CARDIO PH, 33(2), 1999, pp. 248-254
Citations number
34
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
The mechanisms by which red wine polyphenolic compounds (RWPCs) induced end
othelium-dependent relaxation were investigated in rat thoracic aorta rings
with endothelium. RWPCs produced relaxation that was prevented by the nitr
ic oxide (NO) synthase inhibitor, N-omega-nitro-L-arginine-methyl-ester. Th
is relaxation was abolished in the absence of extracellular calcium in the
medium or in the presence of the Ca2+ entry blocker, La3+, but it was not a
ffected by the nonselective K+ channels blocker, tetrabutylammonium. N-Ethy
l-maleimide (NEM), a sulfhydryl alkylating agent, abolished vasorelaxation
produced by RWPCs and acetylcholine but not that produced either by the sar
coendoplasmic reticulum Ca2+-adenosine triphosphatase (ATPase) pump inhibit
or, cyclopyazonic acid (CPA) or the calcium ionophore, ionomycin. Neither p
ertussis toxin (PTX) nor cholera toxin (CTX) inhibited the vasorelaxant eff
ect of RWPC. The effect of RWPC was not affected by the phospholipase C (PL
C) blocker, L-alpha-glycerophospho-D-myo-inositol 4-monophosphate (Gro-Dip)
, and the phospholipase Az pathway blockers, quinacrine and ONO-RS-082. Fin
ally the protein kinase C (PKC) inhibitor, GF 109203X, and tyrosine kinase
inhibitors, tyrphostin A-23 and genistein, did not impair the response to R
WPCs. These results suggest that RWPCs produce endothelium-NO-derived vasor
elaxation through an extracellular Ca2+-dependent mechanism via an NEM-sens
itive pathway. They also show that PTX- or CTX-sensitive G proteins, activa
tion of PLC or PLA(2) pathways, PKC, or tyrosine kinase may not be involved
.