Keef K D, Ross G
Pflugers Arch. 1987 Jul;409(3):308-13. doi: 10.1007/BF00583481.
Contractions induced in isolated ring segments of rabbit coronary arteries by 2-(2-aminoethyl)-pyridine (AEP) were transiently relaxed when KCl, NaCl or sucrose were added to the bathing solution without osmotic correction. When these solutes were added with osmolarity changes minimized by reducing the concentration of another constituent of the medium the relaxations were reduced or abolished. AEP contraction was associated with depolarization and solute-induced relaxation with a lessening of the depolarization. Ouabain depolarized the vessel and diminished both the relaxation and repolarization induced by hyperosmolar addition of NaCl and sucrose to AEP-contracted segments. Sucrose and NaCl also relaxed potassium-induced contractions and their effect was greater at [K]o 25 mM than at [K]o 60 mM. Hyperosmolar relaxation still occurred but was significantly smaller in vessels subjected to prolonged sodium pump inhibition produced by cold storage followed by re-warming in K-free or ouabain-containing solution. It is concluded that hyperosmolar relaxation is mainly due to hyperpolarization and is influenced by the level of membrane potential. The inhibition of hyperosmolar relaxation by ouabain may be due to its depolarizing action.
在不进行渗透压校正的情况下,向浴液中添加氯化钾、氯化钠或蔗糖时,2-(2-氨基乙基)-吡啶(AEP)诱导的兔冠状动脉离体环段收缩会短暂松弛。当通过降低培养基中另一种成分的浓度使渗透压变化最小化的情况下添加这些溶质时,松弛作用会减弱或消失。AEP收缩与去极化有关,而溶质诱导的松弛与去极化程度降低有关。哇巴因使血管去极化,并减弱了向AEP收缩段高渗添加氯化钠和蔗糖所诱导的松弛和复极化。蔗糖和氯化钠也能松弛钾诱导的收缩,且在细胞外钾浓度为25 mM时其作用比在细胞外钾浓度为60 mM时更大。高渗松弛仍然会发生,但在经过冷藏后在无钾或含哇巴因的溶液中复温而导致钠泵长期受抑制的血管中,高渗松弛明显较小。得出的结论是,高渗松弛主要是由于超极化引起的,并且受膜电位水平的影响。哇巴因对高渗松弛的抑制作用可能是由于其去极化作用。