Abstract

Wine consumption is correlated with a reduced incidence of cardiovascular disease. Experimental model systems have demonstrated that wine reduces platelet reactivity, thrombosis, and vasoconstriction. The objective of this investigation was to determine if a single mechanism could mediate these cardioprotective effects. Prostacyclin and nitric oxide are cell signaling molecules that have been described as inhibitors of vasoconstriction, platelet reactivity, and thrombosis. Endothelial cell release of these molecules was investigated because blood-borne phytochemicals can come in contact with endothelial cells. Cabernet Sauvignon, alcoholized and dealcholized, stimulated bovine aortic endothelial cell release of prostacyclin but not nitric oxide. In addition, concentrations that significantly increased prostacyclin release were equivalent to those previously published as inducers of vasorelaxation. Prostacyclin release seemed to be dependent on basal or subbasal protein kinase C activity and occurred in the presence of the calcium ionophore ionomycin. The conclusion from this study is that if wine acts in vivo as we observed it to in vitro, the ability of wine to inhibit platelet reactivity, thrombosis, and vasoconstriction could be mediated through the single mechanism of wine-induced prostacyclin release.

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