Objective: To investigate the role of large Ca2+-activated, delayed-rectifier and ATP-sensitive potassium channel in regulating the relaxation induced by nitric oxide (NO) in normal and passively sensitized human airway smooth muscle (HASM) with serum from asthmatic patients. Methods: The effects of NO or/and potassium channel blockers on the tensions of normal and passively sensitized HASM were measured by using nitric oxide donor and potassium blockers, with the isometric tension recording technique. Results: Showed that (1)In the control group and passively sensitized group, Kv blocker (4-AP) cause concentration-dependent augmentation in the contraction induced by histamine (1 ×10-4 mol/L), (P ＜ 0.05), but Glib (1 × 10-2 mol/L)and TEA (1×10-3 mol/L) have no significant effects on the contraction induced by histamine (1×10-4 mol/L). The maximum tension induced by histamine in passively sensitized group is higher than that in the control group (P ＜ 0.05). (2) NO-donor Sodium Nitroprusside (SNP) bring about significant relaxation in normal and passively sensitized HASM rings (P ＜ 0.05). Relaxations of passively sensitized airway rings [ (29.4 ± 3.3)％ ] were significant less than those of normal HASM rings [ (44.1 ± 10.2)％ ], (P ＜0.05).(3) Glib(1×10-2 mol/L)have no significant effect on the relaxations induced by SNP(1×10-4 mol/L). 4-AP(1×10-2 mol/L) inhibited relaxation induced by SNP (1×10-4 mol/L), (P ＜ 0.01). TEA (1×10-3 mol/L) inhibited relaxation induced by SNP (1×10-4mol/L) (P ＜ 0.05), and the inhibiting effect in passively sensitized HASM rings were significant less than in normal HASM, (P ＜0.05). Conclusion: It was concluded that SNP(NO-donor) relaxed the contraction of HASM partly via BKca channel opening. In passively sensitized HASM in vitro, the relaxation of SNP decreased compared with control group, which might be associated with the down-regulating activity of BKca in passively sensitized HASM.