Ca²⁺ dependent contractions of urethral smooth muscle (USM) prevent leakage of urine during bladder filling. In rabbit and pig, USM contraction relies on Ca²⁺ influx through L-type Ca²⁺ channels (Brading, 2006), and in rabbit this requires USM depolarization via Ca²⁺ activated-Cl^– channels (Ano1) (Fedigan et al., 2017). Studies in mice demonstrated L-type channel inhibitors do not affect phenylephrine (PE) responses in male USM, but store-operated-Ca²⁺-entry (SOCE) via Orai channels was critical (Drumm et al., 2018). However, this study only examined L-type channel inhibitors on responses to supramaximal PE doses (10 µM). Thus, contributions of L-type or Ano1 channels by lower (more physiologically relevant) PE concentrations or nerve stimulation cannot be ruled out. We sought to examine potential roles for L-type and Ano1 channels in regulating male mouse USM across a range of PE concentrations and electrical field stimulation (EFS) frequencies. Intact USM rings from wildtype male C57 mice were mounted on an isometric force transducer inside a heated (37^oC) organ bath, perfused with oxygenated Krebs solution. Contractions and relaxations of USM were monitored using LabScribe. Tissues were stretched to an initial 2 mN of tension and equilibrated for 1 hour before experimentation. EFS was delivered via two platinum electrodes either side of USM rings, at 1, 2, 5, 10, 20 Hz for 30 sec. USM rings contracted in response to PE (30nM – 30 µM) in a concentration dependent manner, with an EC₅₀ of 1.3 µM (n=60). EFS in the presence of L-NNA (nNOS synthase inhibitor), to prevent relaxations of USM due to nitric oxide release, evoked contractions whose amplitude was frequency dependent, with 20 Hz EFS evoking responses 80% larger than those at 2 Hz (n=113). The L-type channel activator FPL 64176 (300 nM) slightly (but significantly) increased the area under the curve (AUC) of PE-induced contractions (e.g. 1 µM PE AUC increased 24.8% in FPL, P<0.05, n=6), without affecting EC₅₀. Similarly, EFS response amplitude was increased by FPL, e.g., contractions at 10 Hz increased 10% (n=6, P<0.05). FPL effects were reversed by the L-type channel inhibitor nifedipine (1 µM, n=6, P<0.05), but nifedipine failed to significantly affect control PE or EFS responses (n=6, P<0.05) at any PE concentration or EFS frequency. In contrast, the Orai Ca²⁺ channel inhibitor GSK 7975A (10 µM), reduced EFS-induced contraction amplitude by 50% at all frequencies (n=13, P<0.005). Upon subsequent addition of nifedipine in the continued presence of GSK 7975A, there was a further 10 – 20% reduction in residual EFS-induced contractions (n=13, p<0.05). The Ano1 channel activator Eact (10 µM) and antagonist Ani9 (3 µM) failed to affect PE dose-response curves or EFS responses at any frequency (n=6, P>0.05). Furthermore, nifedipine sensitive components of EFS-induced responses (unmasked when Orai channels were inhibited) were unaffected by Ani9 (n=6, P>0.05). In conclusion, in male USM, L-type channels can be activated by appropriate agonists (FPL) but inhibition of these channels does not affect PE or EFS responses under normal conditions. Ca²⁺ influx via SOCE is the dominant Ca²⁺ influx pathway required for male USM contraction.