In canine bronchial smooth muscle (BSM), spasmogens evoke oscillations in membrane potential ("slow waves"). The depolarizing phase of the slow waves is mediated by voltage-dependent Ca²⁺ channels; we examined the roles played by Cl and K⁺ currents and Na⁺-K⁺-ATPase activity in mediating the repolarizing phase. Slow waves were evoked using tetraethylammonium (25 mM) in the presence or absence of niflumic acid (100 µM; Cl channel blocker) or ouabain (10 µM; block Na⁺-K⁺-ATPase) or after elevating external K⁺ concentration ([K⁺]) to 36 mM (to block K⁺ currents); curve fitting was performed to quantitate the rates of rise/fall and frequency under these conditions. Slow waves were markedly slowed, and eventually abolished, by niflumic acid but were unaffected by ouabain or high [K⁺]. Electrically evoked slow waves were also blocked in similar fashion by niflumic acid. We conclude that the repolarization phase is mediated by Ca²⁺-dependent Cl currents. This information, together with our earlier finding that the depolarizing phase is due to voltage-dependent Ca²⁺ current, suggests that slow waves in canine BSM involve alternating opening and closing of Ca²⁺ and Cl channels.