Palytoxin-induced endothelium-dependent relaxation in the isolated rat aorta

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Abstract
Summary The effects of a potent marine toxin, palytoxin (PTX), were investigated on the contractile responses in the isolated rat aorta with or without endothelium. PTX in the concentrations of 10−13–10−11 mol/l showed little effect on the resting tension of the vessel with or without endothelium. PTX, 10−10 mol/l, induced a small contraction in the aorta without endothelium but not in the aorta with endothelium. When added during the sustained contraction induced by 10−7 mol/l norepinephrine, 10−12 mol/l PTX sometimes (6 out of 43 strips) augmented the norepinephrine-induced contraction whereas 10 −11–10−10 mol/l PTX induced a biphasic response which was composed of a transient augmentation followed by a relaxation. These effects of PTX were not observed in the aorta without endothelium. Influencesof atropine (10−6 mol/l), indomethacin (2.5 × 10−5 mol/l), methylene blue (5 × 10−6 mol/l), hydroquinone (10−4 mol/l), phenidone (5 × 10−5 mol/l), hemoglobin (10−6 mol/l) and p-bromophenacyl bromide (5 × 10−5 mol/l) on the PTX (10−10 mol/l) induced responses were examined. Methylene blue, hydroquinone, phenidone, hemoglobin and p-bromophenacyl bromide inhibited both the PTX-induced augmentation and relaxation of the norepinephrine-induced contraction. The endothelium-dependent relaxation due to 3 × 10−7 mol/l carbachol was inhibited by atropine, methylene blue, hydroquinone, phenidone, hemoglobin and p-bromophenacyl bromide. These results suggest that PTX acts on the endothelium, modifies the synthesis or release of endothelium-derived relaxing factor and thus changes the contractile response to norepinephrine in rat aorta.