The role of potassium channels in the nitric oxide-induced relaxation of human airway smooth muscle of passively sensitization by serum from allergic asthmatic patients

INTRODUCTIONNitric Oxide (NO), the major endothelium-de-rived relaxing factor (EDRF), can relax thesmooth muscle of airway, vascular and gastroin-testinal. Clinically, nitric oxide (NO) is widely usedas a pulmonary vaso-and bronchodilator agent. Inprevious study, we found that NO relaxed the con-traction of airway smooth muscle partly via potassi-um channel (most of BKca channel) opening inrats [1]. Another animal studies indicated the same re-sults [2] , But there is scarce evidence…

The role of potassium channels in the nitric oxide-induced relaxation of human airway smooth muscle of passively sensitization by serum from allergic asthmatic patients

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.