Properties of spontaneous inward currents recorded in smooth muscle cells isolated from the rabbit portal vein.

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Abstract
1. Characteristics of spontaneous transient inward currents (STICs) which produced membrane depolarization were analysed with the perforated patch technique in single smooth muscle cells isolated from the rabbit portal vein. 2. In K(+)-free solutions the amplitude of STICs was linearly related to membrane potential and the reversal potential (Er) was -3.0 +/- 0.9 mV. Replacement of external NaCl with NaI shifted Er to -40.0 +/- 1.0 mV. Substitution of external NaCl by NaSCN also moved Er to negative values but replacement of sodium with Tris and choline did not change Er. It is concluded that STICs are generated by an increase in chloride conductance. 3. STICs were abolished or reduced by the chloride channel antagonists anthracene-9-carboxylic acid (1 mM) and 4-acetamido-4'-isothiocyanato-2,2'- stilbene-disulphonic acid (2 mM). 4. STICs were blocked by noradrenaline and caffeine which deplete intracellular calcium stores. This effect was reversible and this result indicates that the primary trigger for STICs is calcium released from intracellular stores and therefore STICs are calcium-activated chloride currents (ICl(Ca)). 5. Removal of calcium from the bathing solution abolished STICs in six out of seven cells but STICs persisted in Ca(2+)-free solution in one cell. When STICs were abolished in Ca(2+)-free external solution the size of the internal calcium store, as estimated from the noradrenaline-induced ICl(Ca), was not altered. It appears that an influx of calcium is usually necessary for STICs to be observed. 6. The frequency and amplitude of STICs were not altered by the voltage-dependent calcium channel antagonist cadmium (1 mM). However, in some quiescent cells influx of calcium through voltage-dependent channels did activate STICs. 7. It was concluded that in isolated portal vein cells STICs represent a Ca(2+)-activated chloride current which leads to spontaneous depolarization of the membrane and may play an important physiological or pathophysiological role to produce smooth muscle contraction.