The effects of various K(+) channel blockers on the spontaneous electrical activity of the smooth muscle cells of the ureter still attached to its primary pacemaker regions were investigated using standard intracellular microelectrode recording techniques. Spontaneous action potentials in the ureter were complex, consisting of an initial rapidly rising spike which was followed by a period of membrane oscillation, a quiescent plateau phase and terminated by an abrupt repolarisation and an after-hyperpolarisation with a peak "diastolic" potential of -66 mV. This after-hyperpolarization decayed slowly over 5-20 s until the underlying triggering potentials achieved threshold for another action potential discharge. Application of the Ca(2+)-entry blocker, nifedipine (1 mu;M), blocked action potential discharge within 2-5 min, after which the membrane settled at a potential of -55 mV. 4-Aminopyridine (4-AP)(1 mM for 2 min) and Ba(2+) (100 mu;M for 2 min) both depolarized significantly the diastolic potential. In 4-AP, this membrane depolarisation was associated with a decreased amplitude of the initial spike and an increase in the half-amplitude duration. In contrast, tetraethylammonium (TEA) (0.5 mM for 2 min) only increased the frequency and half-amplitude duration of these ureteric action potentials. Apamin (200 nM), Cs(+) (1 mM) and glibenclamide (1 microM) had no significant effects on any parameters of the ureteric action potential. It was concluded that the refractory period of the spontaneous action potentials in the whole-mount preparation of the upper urinary tract was determined by the opening of at least three K(+) channel populations: large conductance ('maxi K') Ca(2+)-activated K(+) channels; Ca(2+)-insensitive transiently opening K(+) (I(Kto)) channels and K(+)-selective inward rectifier channels.