We investigated the ion currents in canine bronchial arterial smooth muscle using patch clamp techniques. Outward currents were suppressed by TEA (1^-10 mM), charybdotoxin (10^-6 M), nifedipine (10^-6 M) or removal of external Ca²⁺, but not by 4-AP (5 mM). When these were blocked, voltage steps evoked inward currents with characteristics of L-type Ca²⁺ current: (i) activation which was voltage-dependent (threshold and maximal at -50 and -10 mV, respectively); (ii) inactivation which was time-dependent and voltage-dependent (V_0.5 of -26±22 mV); (iii) blockade by nifedipine (10^-6 M). The thromboxane mimetic U46619 (10^-6 M) caused a marked augmentation of outward K⁺ current lasting only 10-20 seconds, followed by significant suppression of the K⁺ current lasting several minutes. Phenylephrine (10^-4 M) also suppressed the K⁺ current but did not cause the initial transient augmentation. None of these 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.