Calcium-gated chloride currents (IClCa) have been recorded in a number of different in smooth muscle cell types predominantly from non-murine species. As future molecular studies necessitate the development of a murine model the goal of the present study was to characterize the biophysiological and pharmacological properties of sustained IClCa in murine aortic myocytes. These characteristics were then compared to IClCa in the rabbit pulmonary artery (rPA) myocytes, which have been investigated extensively, to determine if there are any differences in the recorded current. Balb/c mice (6-8 wk old) were killed by cervical dislocation. Thoracic aorta smooth muscle cells were obtained by enzymatic dispersion. Recordings were made using the whole cell voltage-clamp technique with an external solution of (mM): NaCl 126, MgCl ₂ 1.2, CaCl ₂ 1.5, glucose 11, HEPES 10, TEA-Cl 10, adjusted to pH 7.2 with NaOH. The pipette solution contained (mM): TEA-Cl 20, CsCl 106, MgCl ₂ 1.1, HEPES 10, Na ₂-GTP 0.2, Na ₂-ATP 3, BAPTA 10 and 7.8 mM CaCl ₂. Similar to IClCa in rPA myocytes pipette solutions containing 500 nM free [Ca²⁺]_i activated a sustained inward current at 50 mV that exhibited distinctive, voltage dependent kinetics. This was manifest as an increase in the outward current upon stepping to +70 mV so the mean current increased from 35 ± 1.1pA to 110 ± 2.6 pA over the 1.5 s step (n = 10). Repolarisation to 80 mV evoked an inward current with a mean amplitude of 175 ± 3.5 pA, which declined exponentially (mean t = 57 ± 0.5 ms, n = 10). Stationary noise analysis of the current at the end of a test step to different potentials produced a mean single-channel conductance of 1.6 ± 0.15 pS and 1834 ± 498 channels (n = 5). The reversal potential of IClCa was close to the theoretical equilibrium potential ECl of 0 mV and was shifted by replacement of external Cl- by SCN- by 28.8 ± 2.3 mV (n = 3). Niflumic acid (100 µM) produced a complete but transient inhibition of IClCa, which was followed by a prominent increase to greater than control levels. Antracene-9-carboxylate (500 µM) produced inhibition of currents at +70 mV and increased the inward current upon repolarisation to 80 mV by 173.5 ± 74.3 pA (n = 3). These effects were similar to those observed in rPA myocytes. NPPB at 100 µM had no apparent effect on IClCa in these cells. Rapid rundown of IClCa was not observed in aortic myocytes unlike rPA cells but a slow runup, similar to that found in rPA, occurred in the absence of intracellular ATP. In conclusion, murine aortic myocytes displayed IClCa with similar pharmacological and biophysical properties to those possessed by rPA myocytes but showed notable differences in terms of regulation.