BACKGROUND AND OBJECTIVES: The non-depolarizing muscle relaxant vecuronium 
inhibits contraction by competitive inhibition of postsynaptic acetylcholine 
receptors (AchRs), which decreases the number of quanta released per impulse in 
response to 50 Hz stimulation. The specific role of calcium influx through 
L-type calcium channels is the promotion of endocytosis and vesicle recycling 
during high-frequency stimulation. Vecuronium also induces four pulse tetanic 
fade, a proxy measure of decreased quanta release. We examined whether 
vecuronium suppresses neuromuscular transmission during high-frequency 
stimulation by inhibiting presynaptic L-type calcium channels.
METHODS: Fifty male Sprague-Dawley rats were divided into five treatment groups: 
unstimulated control group, α-bungarotoxin (BTX) group, nifedipine group, 
vecuronium group, and nifedipine plus vecuronium group. Rat phrenic 
nerve-diaphragm neuromuscular juctions were stimulated at 50 Hz and field 
excitatory post-synaptic potentials (fEPSPs) were recorded. Expression levels of 
the presynaptic Ca(2+)-binding, protein synaptotagmin 1, and the presynaptic 
plasma membrane protein, syntaxin 1, were measured by Western blots.
RESULTS: The fEPSPs evoked by 50 Hz stimulus trains were decreased by 
vecuronium, nifedipine, and by vecuronium plus nifedipine. Nifedipine, an L-type 
calcium channel blocker, reduced the expression of synaptogamin and syntaxin and 
blocked the suppressive effect of vecuronium, suggesting that both agents 
inhibit presynaptic L-type calcium channels.
CONCLUSIONS: Vecuronium which blocked L-type calcium channels may suppress 
activity of the α(3)β(2) nAChR subunit, which exists in the presynaptic membrane 
and enhances quantal release. This α(3)β(2) nAChR-mediated positive feedback 
effect may be facilitated by L-type Ca(2+) channel activity under high-frequency 
stimulation. Vecuronium may disrupt this positive feedback cycle, leading to 
suppression of fEPSPs. Vercuronium may reduce neuromuscular transmission through 
presynaptic and postsynaptic mechanisms.