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Department of Pharmacology and Clinical Pharmacology, St George's Hospital Medical School, London.

1. The time course of spontaneous calcium-activated chloride currents was studied with the perforated patch technique in freshly dispersed smooth muscle cells from the rabbit portal vein. 2. In potassium-containing solutions the spontaneous transient outward current (STOC, a calcium-activated potassium current) was more commonly recorded than spontaneous transient inward currents (STICs, a calcium-activated chloride current). In addition the duration of STOCs was much briefer (about 100 ms) than the duration of STICs (about 400 ms). 3. The decay of STICs could be described by a single exponential but the STOC decay appeared to be more complex. The decay time constant of STICs was not determined significantly by amplitude. 4. The time constant of decay of STICs (tau) was 86 ms at -50 mV and was increased by depolarization. Between -90 and +50 mV the relationship between tau and membrane potential was exponential and tau changed e-fold for a change of membrane potential of 120 mV. 5. The I-V relationship of STIC amplitude was linear between -10 and +50 mV but at more negative potentials the chord conductance was reduced and the I-V relationship exhibited negative slope conductance between -50 and -90 mV. 6. There was good agreement between the STIC tau values and the exponential relaxations to voltage steps evoked during caffeine-induced calcium-activated chloride currents. 7. In the presence of the chloride channel blocking agent anthracene-9-carboxylic acid the STIC amplitude was reduced and tau was increased. This effect was voltage dependent with a much greater effect at positive potentials. 8. The evidence suggests that the decay of STICs represents closure of chloride channels and tau approximates to the channel mean open time.

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