Voltage-gated sodium (NaV) channels have been discovered in phasic smooth muscles exhibiting spontaneous electrical activities. However, they have not been discovered in corpus cavernosum, a phasic tissue type known to function as a syncytium. We report, for the first time, fast voltage-dependent sodium current in mouse corpus cavernosum smooth muscle (CCSM).  C57BL/6 mice were humanely euthanised in accordance with European Union legislation and the approval of Dundalk Institute of Technology Animal Use and Care Committee. CCSM cells were isolated using collagenase-proteinase mixture. Currents were recorded at room temperature using the whole cell patch-clamp technique. Isometric tension recordings were performed to study CCSM tissue activity. Six cells from 6 animals were used in each data set. When cells were voltage clamped at -100 mV and subjected to depolarising pulses from -80 to +50 mV fast voltage-dependent inward currents were observed.  These were determined to be sodium current, as evidenced by a 95% reduction in amplitude when external sodium concentration was reduced from 130 mM to 13 mM (p<0.05, paired t-test). At least two sub-types of NaV currents were distinguished on the basis of TTX sensitivity: ‘TTX-sensitive’ and ‘TTX-insensitive’. In the former, the mean IC50 was 10 nM (95% CI ranged from 7 to 15 nM), while in the latter, the concentration-response curve was clearly biphasic, with  IC50  of 14 nM and 672 nM (95% CI range from 9 nM to 59 nM and 445 nM to 6 μM, respectively). The two groups had different activation V1/2s, at -28 ± 12 mV and -39 ± 1 mV for the TTX-sensitive and -insensitive currents, respectively (p<0.05, extra sum of squares F test, Graphpad Prism). They also had different inactivation V­1/2s, at -71 ± 1 mV and -78 ± 1 mV for the TTX-sensitive and -insensitive currents, respectively (p<0.05, extra sum of squares F test, Graphpad Prism). These findings suggest that the two populations of NaV current can be separated based on their steady state voltage-dependent activation and inactivation kinetics. Although, veratridine 30 μM, an agonist of NaV channels, reduced the peak current by 20% (p<0.05, paired t-test), it slowed inactivation, resulting in a 7-fold increase in sustained current amplitude (-20 ± 12 to -145 ± 41 pA; p<0.05, paired t-test). Under current clamp conditions, the mean duration of evoked action potentials was increased from 0.2 ± 0.1 s to 1.2 ± 0.3 s by veratridine, and this was reduced to 0.1 ± 0.02 s by 10 μM TTX (p<0.05, ANOVA and Tukey’s post hoc test). Isometric tension experiments were performed in a drug cocktail to block the effects of endogenous neurotransmitters (phentolamine 3 μM, L-NOARG 100 μM, ab-methyleneATP 10 μM, and atropine 1 μM). Under these conditions, veratridine (10 μM) induced a series of phasic contractions in CCSM tissue strips that were abolished by TTX (100 nM, p<0.05, ANOVA and Tukey’s post hoc test). These findings suggest that NaV channels could contribute to the mechanisms of detumescence, and potentially serve as a clinically relevant target for pharmaceutical intervention.