The bronchial vasculature plays an important role in airway physiology and pathophysiology. We investigated the ion currents in canine bronchial smooth muscle cells using patch-clamp techniques. Sustained outward K⁺ current evoked by step depolarizations was significantly inhibited by tetraethylamonium (1 and 10 mM) or by charybdotoxin (10⁶ M) but was not significantly affected by 4-aminopyridine (1 or 5 mM), suggesting that it was primarily a Ca²⁺-activated K⁺ current. Consistent with this, the K⁺ current was markedly increased by raising external Ca²⁺ to 4 mM but was decreased by nifedipine (10⁶ M) or by removing external Ca²⁺. When K⁺ currents were blocked (by Cs⁺ in the pipette), step depolarizations evoked transient inward currents with characteristics of L-type Ca²⁺ current as follows: 1) activation that was voltage dependent (threshold and maximal at 50 and 10 mV, respectively); 2) inactivation that was time dependent and voltage dependent (voltage causing 50% maximal inactivation of 26 ± 22 mV); and 3) blockade by nifedipine (10⁶ M). The thromboxane mimetic U-46619 (10⁶ M) caused a marked augmentation of outward K⁺ current (as did 10 mM caffeine) lasting only 10-20 s; this was followed by significant suppression of the K⁺ current lasting several minutes. Phenylephrine (10⁴ M) also suppressed the K⁺ current to a similar degree but did not cause the initial transient augmentation. None of these three agonists elicited inward current of any kind. We conclude that bronchial arterial smooth muscle expresses Ca²⁺-dependent K⁺ channels and voltage-dependent Ca²⁺ channels and that its excitation does not involve activation of Cl channels.