ABSTRACT
2,3-Butanedione monoxime (BDM) has been reported to selectively block crossbridge interaction in skeletal and cardiac muscle and BDM has been shown to cause a dose-dependent decrease in smooth muscle maximum tension development (Po). With the relatively recent descriptions of at least two functionally different types of crossbridges (those recruited early in contraction and then fairly rapidly--within 30% of the muscles' contraction time--replaced by very slowly-cycling or "latch" crossbridges), it became important to know whether BDM is a specific inhibitor of one type of crossbridge or the other. In this study it was shown that 7.5 mM BDM had an even greater affect on maximum shortening ability (delta Lmax) having decreased the tracheal smooth muscle delta Lmax by 47%. BDM treatment did not alter "transition time (tT; defined arbitrarily as the time in contraction at which a functionally significant number of slowly-cycling bridges have replaced rapidly-cycling bridges)" in tracheal smooth muscle. Velocity of shortening early in contraction i.e. prior to tT, was decreased by 48%, while velocity late in contraction i.e. post tT, was not decreased with BDM treatment. BDM caused a decrease in maximum load bearing capacity, or maximum force potential (MFP), at all times in contracting tracheal smooth muscle. This investigation supports the suggestion that BDM inhibits crossbridge cycling rate in smooth muscle. In particular BDM appears to specifically inhibit rapidly-cycling crossbridges or their control as it has no apparent affect on cycling rate of very slowly-cycling or "latch" crossbridges in tracheal smooth muscle.
