Planta Med 1998; 64(1): 18-21
DOI: 10.1055/s-2006-957358
Papers
Pharmacology
© Georg Thieme Verlag Stuttgart · New York

Effects of Boldine on Mouse Diaphragm and Sarcoplasmic Reticulum Vesicles Isolated from Skeletal Muscle

Jaw-Jou Kang, Yu-Wen Cheng
  • Institute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan, R.O.C.
Further Information

Publication History

1997

1997

Publication Date:
04 January 2007 (online)

Abstract

The effects of boldine [(S)-2,9-dihydroxy-1,10-dimethoxyaporphine], a major alkaloid in the leaves and bark of boldo (Peumus boldus Mol.), on skeletal muscle were studied using mouse diaphragm and isolated sarcoplasmic reticulum membrane vesicles. Boldine, at 10-200 µM, has little effect on the muscle-evoked twitches; however, the ryanodine-induced contracture was potentiated dose-dependently. At higher concentrations of 300 µM, boldine by itself induced muscle contracture of two phases, which were caused by the influx of extracellular Ca2+ and induction of Ca2+ release from the internal Ca2+ storage site, the sarcoplasmic reticulum, respectively. When tested with isolated sarcoplasmic reticulum membrane vesicles, boldine dose-dependently induced Ca2+ release from actively loaded sarcoplasmic reticulum vesicles isolated from skeletal muscle of rabbit or rat which was inhibited by ruthenium red, suggesting that the release was through the Ca2+ release channel, also known as the ryanodine receptor. Boldine also dose-dependently increased apparent [3 H]-ryanodine binding with the EC50 value of 50 µM. In conclusion, we have shown that boldine could sensitize the ryanodine receptor and induce Ca2+ release from the internal Ca2+ storage site of skeletal muscle.