title: [The role of delayed rectifier potassium channels in the regulation of bronchial smooth muscle tension in asthmatic rats].
abstract: OBJECTIVE
  To investigate the role of delayed rectifier potassium channels (K(V)) in the regulation of bronchial smooth muscle tension in asthmatic rats and their effects on bronchial reactivity in vitro.
  
  
  METHODS
  By using a specific potassium channel blocker, the bronchial contraction induced by spasmogens was observed in normal and asthmatic rats with the isometric tension recording technique.
  
  
  RESULTS
  (1) K(V) blocker 4-aminopyridine (4-AP) caused concentration-dependent bronchial contraction in vitro. The concentration-response curve to 4-AP in the asthmatic group showed a left displacement with bigger pD(2) (the negative logarithm of the drug concentration causing 50% of maximal effect, 2.58 +/- 0.07, n = 10, P < 0.001) and no change in E(max) [maximal effect, (32 +/- 5) mg/mg, P > 0.05], compared with pD(2) (2.12 +/- 0.04, n = 10) and E(max) [(31 +/- 6) mg/mg] obtained in the control group; (2) In the control group, pre-treatment with 0.1 mmol/L 4-AP displaced the concentration-response curves to ET-1 and histamine to the left. pD(2) (for ET-1 and histamine) before and after 4-AP treatment was 6.27 +/- 0.38, 5.59 +/- 0.27 and 6.80 +/- 0.47, 6.42 +/- 0.14 respectively (P < 0.01). E(max) before and after 4-AP treatment was (36 +/- 8) mg/mg, (36 +/- 8) mg/mg and (40 +/- 8) mg/mg, (39 +/- 9) mg/mg respectively (P > 0.05); (3) In the asthmatic group, pre-treatment with 0.1 mmol/L 4-AP had no effect on the concentration-response curve to ET-1 and histamine. There was no significant difference (P > 0.05) in pD(2) before (6.51 +/- 0.07, 5.86 +/- 0.14 respectively) and after (6.48 +/- 0.16, 5.96 +/- 0.08 respectively) 4-AP treatment, and in E(max) before [(61 +/- 8) mg/mg, (54 +/- 11) mg/mg respectively] and after [(65 +/- 10) mg/mg, (55 +/- 9) mg/mg respectively] 4-AP treatment.
  
  
  CONCLUSIONS
  The activity of K(V) decreases in bronchial smooth muscle isolated from asthmatic rats compared with that obtained from normal ones. This change may be involved in the bronchial hyperreactivity to some spasmogens in vitro in asthmatic rats.
authors.affiliation: Department of Respiratory Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
authors.forename: Xian-sheng
authors.initials: XS
authors.lastname: Liu
authors.forename: Yong-jian
authors.initials: YJ
authors.lastname: Xu
authors.forename: Zhen-xiang
authors.initials: ZX
authors.lastname: Zhang
authors.forename: Chao-qian
authors.initials: CQ
authors.lastname: Li
authors.forename: Dan-lei
authors.initials: DL
authors.lastname: Yang
mesh_terms: D000818:Animals; D001249:Asthma / Q000503:physiopathology*; D001980:Bronchi / Q000503:physiopathology; D051668:Delayed Rectifier Potassium Channels; D004195:Disease Models, Animal; D008297:Male; D009119:Muscle Contraction / Q000502:physiology*; D009130:Muscle, Smooth / Q000503:physiopathology*; D015221:Potassium Channels / Q000502:physiology*; D024642:Potassium Channels, Voltage-Gated; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D051668:Delayed Rectifier Potassium Channels; D015221:Potassium Channels; D024642:Potassium Channels, Voltage-Gated