There is a plethora of data on transient outward currents (A-type, I_A) in various cell types (see review by Amberg et al. 2003) but relatively less is known about I_A in vascular smooth muscle cells. Here we describe the pharmacological, electrophysiological and molecular properties of IA in isolated mouse portal vein (mPV) myocytes. Female BALB/c mice aged 6 to 8 weeks were humanely killed and single mPV cells were obtained by enzymatic dispersion. Recordings were made using the whole-cell voltage-clamp techniques with an external solution of (mM): NaCl 126, KCl 5, MgCl₂ 1, CaCl₂ 0.1, glucose 11, Hepes 10, adjusted to pH 7.2 with NaOH. The internal solution contained (mM): KCl 130, MgCl₂ 1, ATP 2, Hepes 10, EGTA 5, adjusted to pH 7.2 with KOH. Currents were evoked by stepping to various test potentials (VT) from a holding potential of –60 mV or –90 mV. I_A was isolated by subtracting those currents at VT evoked from –60 mV from those with a –90 mV prepulse. Values are mean ± S.E.M. I_A was evoked with an apparent threshold of approximately –40 mV and inactivated rapidly. Peak amplitude at +20 mV was 568 ± 41 pA (n=42). Half voltage of activation was –11 ± 2 mV (slope (k) = 12 ± 3 mV, n=29); and –85 ± 2 mV (k = 4 ± 0 mV, n=11) for inactivation. Time to peak was also voltage dependent, becoming faster with stronger depolarizations, e.g. 4.2 ± 0.2 ms at VT = +20 mV (n=25) but 7.8 ± 0.4 ms at –20 mV (n=26). Current decay was described by a double exponential with fast (τfast) and slow (τslow) components. τfast was 6.3 ± 1.6 ms at +20 (n=13) and 24.2 ± 4.6 ms (n=8) at –40 mV. Application of 5 mM 4-AP had a small effect on I_A and the block was voltage dependent (inhibition was 54.4 ± 5.2% at –40 mV and 29.8 ± 5.9% at +20 mV, n=11). In comparison, flecainide was an effective inhibitor of I_A (IC₅₀ at +20 mV was 0.13 μM, n=4). The KCNQ blocker XE991 (10 μM) also reduced peak current at +20 mV by 32.9 ± 7.5% (n=6). A number of different protein combinations underlie I_A. Quantitative PCR identified relatively abundant transcripts for Kv1.7, Kv4.3 and the accessory genes Kvb3, KCNE2 and KCNE3 (Ohya et al. 2003). These pharmacological and molecular data suggest that the I_A in murine portal vein may reflect a novel combination of gene products.