Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases · 1998
[Inhibition of potassium channel by chronic hypoxia on pulmonary artery smooth muscle cells in rats].
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Xiao X, Chen W, Cheng D
Аннотация
OBJECTIVE: To explore the possible effect of potassium channel in chronic hypoxic pulmonary hypertension.
METHOD: Male Wistar rats were placed in the identical normobaric or hypoxic environmental chamber. In one chamber, rats were maintained in 10% +/- 0.5% O2(by displacement with N2) for 3 weeks, whereas in the other, rats were maintained in air. The single smooth muscle cell was isolated from pulmonary artery (phi 200-700 microns) of Wistar rats with acute enzymatic digestion method. Using patch-clamp technique, we recorded the outward K+ currents in pulmonary artery smooth muscle cells and identified a Ca2+.ATP activated K+ channel (K+Ca-ATP) and a delayed rectifier K+ channel among the outward K+ currents. We compared the activities of Ca2+.ATP activated K+ channel (K+Ca-ATP) or delayed rectifier K+ channel in smooth muscle cells isolated from pulmonary artery of chronic hypoxic and normoxic rats.
RESULT: The activities of Ca2+.ATP activated K+ channel (K+Ca-ATP) and delayed rectifier K+ channel in chronic hypoxic group are much lower than that in normal group (T test, P < 0.01). Cromakalim (10 mmol) caused a marked enhancement of activity of the reduced K+Ca-ATP but not the delayed rectifier K+ channel in rats of hypoxic group.
CONCLUSION: The persistent decrease of potassium channel activity may contribute to setting the development of chronic hypoxic pulmonary hypertension. Cromakalim, one of potassium channel openers, can decrease the pulmonary hypertension induced by chronic hypoxia and may be a new effective drug for treatment of hypoxic pulmonary hypertension.
METHOD: Male Wistar rats were placed in the identical normobaric or hypoxic environmental chamber. In one chamber, rats were maintained in 10% +/- 0.5% O2(by displacement with N2) for 3 weeks, whereas in the other, rats were maintained in air. The single smooth muscle cell was isolated from pulmonary artery (phi 200-700 microns) of Wistar rats with acute enzymatic digestion method. Using patch-clamp technique, we recorded the outward K+ currents in pulmonary artery smooth muscle cells and identified a Ca2+.ATP activated K+ channel (K+Ca-ATP) and a delayed rectifier K+ channel among the outward K+ currents. We compared the activities of Ca2+.ATP activated K+ channel (K+Ca-ATP) or delayed rectifier K+ channel in smooth muscle cells isolated from pulmonary artery of chronic hypoxic and normoxic rats.
RESULT: The activities of Ca2+.ATP activated K+ channel (K+Ca-ATP) and delayed rectifier K+ channel in chronic hypoxic group are much lower than that in normal group (T test, P < 0.01). Cromakalim (10 mmol) caused a marked enhancement of activity of the reduced K+Ca-ATP but not the delayed rectifier K+ channel in rats of hypoxic group.
CONCLUSION: The persistent decrease of potassium channel activity may contribute to setting the development of chronic hypoxic pulmonary hypertension. Cromakalim, one of potassium channel openers, can decrease the pulmonary hypertension induced by chronic hypoxia and may be a new effective drug for treatment of hypoxic pulmonary hypertension.