Vasodilative effect of perillaldehyde on isolated rat aorta

The vasodilative effect of perillaldehyde, one of the major oil components in Perilla frutescens BRITTON, was studied using isolated rat aorta. Perillaldehyde at final concentrations of 0.01 to 1 mM showed dose-dependent relaxation of the aorta contracted by treatment with prostaglandin F2α or norepinephrine. Neither the presence of N^G-nitro-l-arginine methyl ester nor removal of the aortic endothelium affected the vasodilatation, suggesting that perillaldehyde exerts a direct effect on vascular smooth muscle cells. The vasodilative effect of perillaldehyde was not inhibited by pretreatment with a β-adrenergic receptor blocker (propranolol), an inhibitor of phosphodiesterase (theophylline), a delayed rectifier K⁺ channel blocker (tetraethylammonium chloride), or an ATP-sensitive K ⁺ channel blocker (glibenclamide). However, perillaldehyde showed contrasting effects on vasodilatation of the aorta contracted by an influx of extracellular Ca²⁺ - perillaldehyde caused little vasodilatation on the aorta contracted by the Ca²⁺ ionophore A23187, while it inhibited the vasoconstriction induced by treatment with high-concentration K ⁺, which dominantly opened the voltage-dependent Ca²⁺ channel. These results suggest that the vasodilative effect of perillaldehyde is derived from blocking the Ca²⁺ channels.