Fu Zhao-jun, Cheng Hong-wei, Zhang Li-fan, Ma Jin, Zhang Le-ning, Ma Xiao-wu
Space Med Med Eng (Beijing). 2003 Aug;16(4):253-6.
To examine the change of potassium channel function in hindlimb arterial smooth muscle cells in tail-suspended rats and to elucidate the underlying electro-physiological mechanisms responsible for the depressed vascular responsiveness of hindlimb arteries induced by simulated weightlessness.
The contractile responsiveness of femoral arterial rings of 1-wk and 4-wk tail-suspended rats to potassium channel blockers, tetraethylammonium chloride (TEA) and 4-aminopyridine (4-AP), were recorded, and the currents of large conductance calcium-dependent potassium channel (BK(Ca)) and voltage activated potassium channel (Kv) of vascular smooth muscle cells (VSMCs) in saphenous arteries from 1-wk tail-suspended rats were recorded using the whole cell recording mode of patch clamp technique.
The femoral arteries from of 1-wk and 4-wk tail-suspended rats showed a decreased contractile response to 60 mM KCl, and the ratio of their contractile responses induced by TEA or 4-AP to their responses induced by 60 mM KCl increased significantly after 1-wk and 4-wk simulated weightlessness. However no difference was found between 1-wk and 4-wk tail-suspended rats. The whole cell current recording showed that BK(Ca) current densities and K(v) current densities of VSMCs in saphenous artery increased significantly after 1-wk simulated weightlessness.
The contractile response of hindlimb arteries to KCl decreased after simulated weightlessness. The activities of BK(Ca) and K(v) of smooth muscle cells in hindlimb arteries from tail-suspended rats increased, and these changes might be among the electro-physiological mechanisms involved in the depressed vasoreactivity of hindlimb arteries due to simulated weightlessness.
研究尾部悬吊大鼠后肢动脉平滑肌细胞钾通道功能的变化,阐明模拟失重诱导后肢动脉血管反应性降低的潜在电生理机制。
记录1周和4周尾部悬吊大鼠股动脉环对钾通道阻滞剂氯化四乙铵(TEA)和4-氨基吡啶(4-AP)的收缩反应,并采用膜片钳技术的全细胞记录模式记录1周尾部悬吊大鼠隐动脉血管平滑肌细胞(VSMCs)的大电导钙依赖性钾通道(BK(Ca))和电压激活钾通道(Kv)电流。
1周和4周尾部悬吊大鼠的股动脉对60 mM KCl的收缩反应降低,1周和4周模拟失重后,TEA或4-AP诱导的收缩反应与60 mM KCl诱导的收缩反应之比显著增加。然而,1周和4周尾部悬吊大鼠之间未发现差异。全细胞电流记录显示,1周模拟失重后隐动脉VSMCs的BK(Ca)电流密度和K(v)电流密度显著增加。
模拟失重后后肢动脉对KCl的收缩反应降低。尾部悬吊大鼠后肢动脉平滑肌细胞的BK(Ca)和K(v)活性增加,这些变化可能是模拟失重导致后肢动脉血管反应性降低的电生理机制之一。