Key result
Eugenol (1-10 mM) increased resting tension in isolated rat atrial trabeculae in a dose-dependent manner, likely resulting from cooperative activation of cardiac thin filaments due to reduced ATP.
Eugenol increases resting tension in rat atrial trabeculae, likely due to cooperative activation of cardiac thin filaments by strongly attached cross-bridges resulting from reduced ATP concentration.
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May indicate diastolic impairment risk with eugenol; leaves open relevance to human atrial function.
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).
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Olivoto et al. (2014) studied this question. Eugenol was evaluated on Resting tension and atrial ATP content. Eugenol (1-10 mM) increased resting tension in isolated rat atrial trabeculae in a dose-dependent manner, likely resulting from cooperative activation of cardiac thin filaments due to reduced ATP.
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