Analysis of the time course of calcium-activated chloride "tail" currents in rabbit portal vein smooth muscle cells.

The time course of calcium-activated chloride "tail" currents (Itail) in single cells of the rabbit portal vein was studied. These currents were activated by the influx of calcium through voltage-dependent calcium channels (VDCCs). At -50 mV, Itail decayed exponentially with a time constant (tau) of 80-100 ms that was independent of amplitude and was similar to the tau of the decay of spontaneous transient inward currents (STICs; calcium-activated chloride currents). The decays of the STIC and Itail had a similar voltage dependence between -50 and -110 mV and were similarly affected by the chloride channel blocker, niflumic acid. However, at more positive potentials (-20 to +40 mV), Itail was sustained for the duration of the test pulse in most cells, in contrast to STICs which decayed exponentially. At very positive potentials (e.g. +100 mV), when little calcium enters the cell through VDCCs, Itail decayed exponentially. Measurement of calcium current (ICa) at various potentials showed that the VDCCs did not inactivate fully at potentials between -20 and +30 mV. We propose that at negative potentials the decay of Itail is determined by slow gating of the chloride channel, but at positive potentials a sustained Itail is produced by persistent influx of calcium through non-inactivating VDCCs.