Key result
Eugenol induces frog skeletal muscle contractions by releasing SR calcium via ryanodine and heparin-sensitive pathways.
Why the study?
The mechanisms by which eugenol induces muscle contractions via calcium release from the sarcoplasmic reticulum in skinned skeletal muscle fibers were unclear.
Eugenol induces skeletal muscle contraction via Ca(2+) release from the sarcoplasmic reticulum involving both ryanodine receptors and a heparin-sensitive pathway.
No immediate clinical implications from frog skeletal fiber data; leaves open SR Ca2+ mechanisms for cardiac research.
The effects of eugenol on the sarcoplasmic reticulum (SR) and contractile apparatus of chemically skinned skeletal muscle fibers of the frog Rana catesbeiana were investigated. In saponin-skinned fibers, eugenol (5 mmol/L) induced muscle contractions, probably by releasing Ca(2+) from the SR. The Ca(2+)-induced Ca(2+) release blocker ruthenium red (10 micromol/L) inhibited both caffeine- and eugenol-induced muscle contractions. Ryanodine (200 micromol/L), a specific ryanodine receptor/Ca(2+) release channel blocker, promoted complete inhibition of the contractions induced by caffeine, but only partially blocked the contractions induced by eugenol. Heparin (2.5 mg/mL), an inositol 1,4,5-trisphosphate (InsP3) receptor blocker, strongly inhibited the contractions induced by eugenol but had only a small effect on the caffeine-induced contractions. Eugenol neither altered the Ca(2+) sensitivity nor the maximal force in Triton X-100 skinned muscle fibers. These data suggest that muscle contraction induced by eugenol involves at least 2 mechanisms of Ca(2+) release from the SR: one related to the activation of the ryanodine receptors and another through a heparin-sensitive pathway.
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Lofrano‐Alves et al. (2005) studied this question. Eugenol was evaluated on Muscle contractions and Ca(2+) release from the sarcoplasmic reticulum. Eugenol-induced muscle contractions in saponin-skinned frog skeletal muscle fibers involve Ca(2+) release from the sarcoplasmic reticulum via both ryanodine receptors and a heparin-sensitive pathway.
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