Effects of eugenol on resting tension of rat atria

Abstract

In cardiac and skeletal muscle, eugenol (μM range) blocks excitation-contraction coupling. In skeletal muscle, however, larger doses of eugenol (mM range) induce calcium release from the sarcoplasmic reticulum. The effects of eugenol are therefore dependent on its concentration. In this study, we evaluated the effects of eugenol on the contractility of isolated, quiescent atrial trabeculae from male Wistar rats (250-300 g; n=131) and measured atrial ATP content. Eugenol (1, 3, 5, 7, and 10 mM) increased resting tension in a dose-dependent manner. Ryanodine [100 µM; a specific ryanodine receptor (RyR) blocker] and procaine (30 mM; a nonspecific RyR blocker) did not block the increased resting tension induced by eugenol regardless of whether extracellular calcium was present. The myosin-specific inhibitor 2,3-butanedione monoxime (BDM), however, reversed the increase in resting tension induced by eugenol. In Triton-skinned atrial trabeculae, in which all membranes were solubilized, eugenol did not change resting tension, maximum force produced, or the force vs pCa relationship (pCa=-log [Ca2+]). Given that eugenol reduced ATP concentration, the increase in resting tension observed in this study may have resulted from cooperative activation of cardiac thin filaments by strongly attached cross-bridges (rigor state).

Eugenol delays the onset of ouabain‐induced ventricular cardiac arrhythmias in guinea pigs

“…2,3 In the cardiovascular system, several studies in isolated tissue preparation have demonstrated the vasorelaxant properties of eugenol in endothelium-intact aorta preparations, 4,5 and isolated atrial trabeculae. 6 Using human embryonic kidney cells transiently expressing human Na V 1.5, it was shown that eugenol reduced the I Na in a concentration-dependent manner, and also decreased the late component of I Na (I Na,Late ), which shows significant arrhythmic properties. 7 Despite the benefit of heterologous expression system, it does not represent full extent of the pharmacological profile of antiarrhythmic drugs.…”