An inward current in smooth muscle cells (SMCs) of the taenia coli is known to be transferred via potassium channels and nonselective cation channels. The outward current is of a potassium nature and includes several components, Ca-dependent potassium current (I K(Ca) ) and delayed rectifying potassium current (I K(V) ) in particular. Applications of 100 nM paxilline to SMCs of the guinea-pig taenia coli suppressed considerably the outward current and decreased its oscillations; the effect of paxilline reached its maximum in 2 to 3 min from the beginning of application. Analysis of the current-voltage (I-V) relationship observed under conditions of such applications showed that the paxilline-sensitive current is highly dependent on the intracellular Ca 2+ concentration; a change in the I-V slope within a segment of the maximum activation of the calcium current is indicative of this peculiarity. Application of paxilline against the background of the action of 1 mM tetraethylammonium (a nonselective blocker of potassium channels) evoked no additional suppression of the outward current. In most cells, we observed spontaneous outward currents (SOCs). Application of 100 nM paxilline nearly completely blocked high-amplitude SOCs (>10 pA) formed due to activation of big-conductance Ca-dependent potassium channels. At the same time, the frequency of smallamplitude SOCs (<10 pA) practically did not change. Thus, according to the pharmacological and time characteristics, voltage dependence, and sensitivity to the intracellular Ca 2+ concentration, we identified a voltage-operated paxilline-sensitive component in I K(Ca) that is transferred via big-conductance Ca-dependent potassium channels.