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Effects of the compound 2,3 Butanedione monoxime (BDM) on force development have been described in skeletal muscle (Fryer et al., 1988), cardiac muscle (Bergey et al., 1981; West & Stephenson 1989) as well as in smooth muscle (Osterman et al., 1993; Watanabe, 1993). It inhibits contraction acting at different levels: on the contractile mechanism as was shown by Horiuti et al. (1988) and Osterman et al. (1993) and on the excitation-contraction coupling process (Hui & Maylie, 1991; De Armas et al., 1993; Li et al., 1985). In addition to these effects on contractility the drug reduces Ca“ current through L-type Ca2+ channels in cardiac (Coulombe et al., 1990; Chapman, 1992; Ferreira et al., 1993), skeletal muscle (Fryer et al., 1988) and smooth muscle (Lang & Paul, 1991). This reduction obeys to an enhanced voltage dependent inactivation of the channel (Chapman 1992, 1993; Ferreira et al., 1993). Since BDM is a chemical phosphatase, member of a group of oximes with the ability to reactivate cholinesterase after exposure to organo-phosphorous compounds (Wilson & Grinsberg, 1955), it has been suggested that dephosphorylation is the mechanism of action of the drug. Several experimental evidences recently provided are in line with this hypothesis (Chapman, 1993a; Chapman, 1995). |
