Mechanisms Mediating the Vasorelaxing Action of Eugenol, a Pungent Oil, on Rabbit Arterial Tissue

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The inhibitory actions of eugenol on intracellular Ca²⁺ concentration ([Ca²⁺]_i) and the contractions induced by excess extracellular K⁺ concentration ([K⁺]_o) in rabbit thoracic aorta were investigated. Application of excess [K⁺]_o solution (30 - 90 mM) produced contraction and increased the intensity of the Ca²⁺ fluorescence signal. Pretreatment with eugenol (≥0.1 mM) reduced both the amplitude of contraction and the intensity of the Ca²⁺ fluorescence signal, but the contraction was more strongly affected than the [Ca²⁺]_i. Application of eugenol (0.3 mM) to tissue precontracted by 90 mM [K⁺]_o solution (immediately after the removal of the 90 mM [K⁺]_o solution) slowed the decay of the [Ca²⁺]_i signal, but it did not change the rate of relaxation. Carbonyl cyanide m-chlorophenylhydrozone (10 μM), a mitochondrial metabolic inhibitor, produced a reduction in tension despite a slight increase in [Ca²⁺]_i when applied to muscle precontracted by 90 mM [K⁺]_o solution. These results indicate that eugenol relaxes the rabbit thoracic aorta while suppressing the Ca²⁺-sensitivity and both the uptake and extrusion mechanisms for Ca²⁺. To judge from the similarities between its actions and those of metabolic inhibitors, eugenol may produce its actions at least partly through metabolic inhibition.