Our previous study on mouse portal vein (mPV) smooth muscle cells (SMC) revealed that in a subpopulation of cells the L-type Ca²⁺ current was superimposed with a nicardipine resistant component, which had faster activation and inactivation kinetics (Saleh & Greenwood, 2003). The aim of this study was to characterise this fast current and try to decipher its identity. Female BALB/c mice were killed by cervical dislocation and SMC were liberated as previously described (Saleh & Greenwood, 2003). SMC were identified by their characteristic spindle shaped appearance and ability to contract. Currents were recorded in the perforated patch whole cell configuration using a micropipette solution containing 126mM CsCl, 10mM HEPES, 4mM MgCl₂, 5mM Na₂ATP, 5mM EGTA & 600µglµ^-1 amphotericin. The external solution contained 126mM NaCl, 10mM Glucose, 20mM HEPES, 30mM Mannitol, 1.2mM MgCl₂ and 1.5mM CaCl. Data are mean of n cells ± sem.In 23% (23 from 99) of SMC accessed, depolarisation from a holding potential (V_h) of −60mV resulted in a biphasic waveform containing a fast component, which was resistant to the dihydropyridine L-type Ca²⁺ channel antagonist nicardipine, and a further nicardipine sensitive slower component (n= 6). The fast component was also resistant to the inorganic metals Cd²⁺ (n= 3) and Ni²⁺ (n=3) and the T-type Ca²⁺ channel antagonist mibefradil (1µM, n= 3). This current was voltage dependent and had a maximum amplitude (I_MAX) of −68± 15pA, which occurred at +10mV (Vh= −60mV). V_0.5 of inactivation was calculated to be −43± 10mV when V_h was −60mV. The peak amplitude was reached in 5± 1ms, the current was completely inactivated within 16± 2ms with a decay constant of 1.7± 0.2ms (n=5). The fast current was completely abolished by 1µM tetrodotoxin and was also eliminated when external Na⁺ was replaced with equimolar TRIS. These data are consistent with the fast current being a voltage dependent Na⁺ current. Preliminary data from RT- PCR studies support this hypothesis. This study provides definitive evidence for the existence of Na⁺ channels in freshly dispersed SMC of the mPV. Future experiments on the mPV will be conducted to establish the functional role these channels.