Emodin-induced muscle contraction of mouse diaphragm and the involvement of Ca2+ influx and Ca2+ release from sarcoplasmic reticulum

British Journal of Pharmacology
Y W Cheng, J J Kang

Abstract

1. The effects on skeletal muscle of emodin, an anthraquinone, were studied in the mouse isolated diaphragm and sarcoplasmic reticulum (SR) membrane vesicles. 2. Emodin dose-dependently caused muscle contracture, simultaneously depressing twitch amplitude. Neither tubocurarine nor tetrodotoxin blocked the contraction suggesting that it was caused myogenically. 3. The contraction induced by emodin persisted in a Ca2+ free medium with a slight reduction in the maximal force of contraction. The contraction induced by emodin in the Ca2+ free medium was completely blocked when the internal Ca2+ pool of the muscle was depleted by ryanodine. These data suggest that the contraction caused by emodin is due to the release of Ca2+ from the intracellular ryanodine-sensitive pool. 4. In contrast to the effect seen in the Ca2+ free medium, emodin induced a small but consisted contraction in the ryanodine-treated muscle in Krebs medium. The contraction was blocked in the presence of dithiothreitol and was partially blocked by nifedipine, suggesting that oxidation of a sulphhydryl group on the external site of dihydropyridine receptor is involved. 5. Emodin dose-dependently increased Ca2+ release from actively loaded SR vesicles and this effec...Continue Reading

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