Electrically-induced twitch responses of the prostatic segment of vas deferens 
(0.1 Hz, 65 V, 1 ms) are mainly due to the transient presynaptic release of ATP, 
which acts postsynaptically on non-adrenergic receptors to contract smooth 
muscle cells. These responses were fully blocked by nanomolar concentrations of 
the omega-conotoxins GVIA, MVIIA, and MVIIC, most likely by inhibiting Ca2+ 
entry through presynaptic N-type Ca2+ channels controlling the release of ATP. 
Repeated washout of the toxins allowed the recovery of contractions, except for 
omega-conotoxin GVIA, whose inhibitory effects remained unchanged for at least 
60 min. In addition, micromolar concentrations of omega-conotoxin MVIIC were 
unable to protect against the irreversible inhibition of twitch contractions 
induced by nanomolar concentrations of omega-conotoxin GVIA. At low 
extracellular Ca2+ concentrations (1.5 mM), 20 nM of omega-conotoxin GVIA or 
MVIIA inhibited completely the twitch contractions in about 10 min. In 5 mM Ca2+ 
the blockade of twitch contractions after 10 min was 70% for both toxins. In 1.5 
mM Ca2+ omega-conotoxin MVIIC (1 microM) inhibited completely the twitch 
contraction after 10 min. In 5 mM Ca2+ blockade developed very slowly and was 
very poor after 30 min, omega-conotoxin MVIIC depressed the response by only 
20%. These results are compatible with the idea that the three omega-conotoxins 
block the purinergic neurotransmission of the vas deferens by acting on 
presynaptic N-type voltage-dependent Ca2+ channels. However, omega-conotoxin 
MVIIC seems to bind to sites different from those recognised by omega-conotoxin 
GVIA and MVIIA, which are markedly differentiated by their Ca2+ requirements for 
binding to their receptors.