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).
Highlights
In cardiac muscle, excitation-contraction coupling (ECC) is mediated by Ca2+ influx through voltage-gated Ca2+ channels
We demonstrated that eugenol increased resting tension in a concentration-dependent manner
Because it has been demonstrated that eugenol blocks an L-type calcium channel [8], and because the increase in the resting tension was not blocked by calcium-free Ringer solution, it is unlikely that this effect was due to calcium inflow
Summary
Excitation-contraction coupling (ECC) is mediated by Ca2+ influx through voltage-gated Ca2+ channels (dihydropyridine receptors, DHPRs). This limited Ca2+ entry triggers a massive Ca2+-induced Ca2+ release (CICR) from the sarcoplasmic reticulum (SR), a process that leads to activation of contractile proteins and cardiac muscle contraction [1]. It is well established that CICR is mediated by the ryanodine receptors (RyRs) of Ca2+ release channels on the membrane of the SR [2,3]. Experimental studies have demonstrated that eugenol has a broad range of biological effects. The authors suggest that this effect is likely due to blockage of the L-type calcium channel
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