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  • Title: [The effect of nitric oxide on potassium channels of bronchial smooth muscle cells from asthmatic rats].
    Author: Gao YD, Xiong SD, Xu YJ, Zhang ZX, Liu XS.
    Journal: Zhonghua Jie He He Hu Xi Za Zhi; 2003 Oct; 26(10):615-8. PubMed ID: 14633445.
    Abstract:
    OBJECTIVE: To investigate the effect of nitric oxide (NO) on resting membrane potential (Em) and potassium currents of bronchial smooth muscle cells (BSMC) from asthmatic rat models. METHODS: Sixteen male SD rats were randomly divided into two groups: a control group and an asthmatic model group. Single BSMC was obtained by acute enzyme-digestion separation method. All experiments were conducted in conventional whole-cell configuration of patch clamp technique. Em currents of Ca2+ activated potassium channels (BKCa) and voltage-dependent potassium channel (Kv) of two groups were separately measured, and the changes of The resting Em and potassium currents of BSMC before and after addition of NO donor sodium nitroprusside (SNP) were also measured. RESULTS: (1) The Em of the asthmatic model group [(-29 +/- 6) mV, n = 12] was significantly lower than that of the control group [(-35 +/- 6) mV, n = 15, P < 0.05]; SNP significantly increased Em of the asthmatic model group to [(-38 +/- 7) mV, n = 12, (P < 0.0 1)], there is no significant difference of Em between normal group and that of asthmatic model group after SNP treatment (P > 0.05), which meant that SNP could repolarize BSMC to normal. (2) The mean current density of BKCa from asthmatic model group [(44 +/- 17) pA/pF, n = 8] under pulse protocol was significantly lower than that of the control group [(73 +/- 20) pA/pF, n = 10, P < 0.01], and SNP significantly increased the mean current density of the asthmatic model group to [(79 +/- 16) pA/pF, n = 10, P < 0.01], which was close to control group (P > 0.05); under ramp protocol, the current densities of control and asthmatic model group were [(75 +/- 19) pA/pF, n = 10] and [(46 +/- 16) pA/pF, n = 8] respectively, there was significant difference between two groups (P < 0.01), SNP treatment significantly increased current density of asthmatic model group to [(82 +/- 21) pA/pF, n = 8, P < 0.01]. (3) The mean current density of Kv of the asthmatic model group [(32 +/- 9) pA/pF, n = 8] under pulse protocol was significantly lower than that of the control group [(58 +/- 10) pA/pF, n = 8, P < 0.05], and SNP significantly increased the mean current density of Kv of the asthmatic model group to [(45 +/- 13) pA/pF, n = 8, P < 0.05]. Under ramp protocol, current density of Kv of asthmatic model group was [(38 +/- 11) pA/pF, n = 8], which was significantly lower than that of control group [(62 +/- 14) pA/pF, n = 8, P < 0.05], SNP treatment significantly increased Kv current density of asthmatic model group to [(53 +/- 9) pA/pF, n = 8, P < 0.05]. there was a similar change. CONCLUSIONS: SNP can improve the resting membrane potential of BSMC from rat asthmatic models and increase the potassium channel activity of BSMC, which is impaired in asthma status. The result suggests that potassium channel mediates the relaxation effect of NO on asthmatic airway smooth muscle.
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