细胞外高浓度钾离子对人血小板中86Rb+外流的影响：钠/钾/2氯协同转运的证据。

Na+/K+/2Cl- co-transport mediates a bidirectional symport of Na+, K+ and Cl-. The important properties of the co-transport system are its requirement for Na+, K+ and Cl- and its inhibition by loop diuretics such as bumetanide. This co-transporter has been described in a number of animal and human tissues. However, its presence in human platelets, although inferred, has not been demonstrated directly. 2. We have studied the efflux of 86Rb+ (a marker for K+) from Rb(+)-loaded platelets, and have defined their response to stimulation by high concentrations of external K+. 3. KCl (30-120 mmol/l) stimulated a concentration-dependent increase in 86Rb+ efflux from the platelets. This efflux was completely inhibited by bumetanide (10 mumol/l) but was insensitive to ouabain and R(+)-[(dihydroindenyl)oxy]alkanoic acid. It also required Cl- in the external medium, but did not depend on the presence of extracellular Na+. 4. These observations suggest that 86Rb+ efflux from platelets stimulated by external K+ occurs via Na+/K+/2Cl- co-transport acting in a K+/K+ (K+/Rb+) exchange mode. 5. Non-stimulated efflux of 86Rb+ from the platelets (i.e. in the presence of 5 mmol/l K+) had the characteristics of Na+/K+/2Cl- co-transport acting in normal mode.

Na⁺/K⁺/2Cl⁻共转运介导Na⁺、K⁺和Cl⁻的双向同向转运。该共转运系统的重要特性是对Na⁺、K⁺和Cl⁻的需求以及对布美他尼等袢利尿剂的抑制作用。这种共转运体已在多种动物和人体组织中被描述。然而，其在人血小板中的存在，尽管是推测的，但尚未得到直接证实。2. 我们研究了研究了从负载Rb⁺的血小板中86Rb⁺（K⁺的标志物）的流出，并确定了它们对高浓度外部K⁺刺激的反应。3. KCl（30 - 120 mmol/L）刺激血小板中86Rb⁺流出呈浓度依赖性增加。这种流出被布美他尼（10 μmol/L）完全抑制，但对哇巴因和R⁺-[(二氢茚基)氧基]链烷酸不敏感。它还需要外部介质中的Cl⁻，但不依赖于细胞外Na⁺的存在。4. 这些观察结果表明，外部K⁺刺激血小板中86Rb⁺的流出是通过以K⁺/K⁺（K⁺/Rb⁺）交换模式起作用的Na⁺/K⁺/2Cl⁻共转运发生的。5. 血小板中86Rb⁺的非刺激流出（即在5 mmol/L K⁺存在下）具有正常模式下Na⁺/K⁺/2Cl⁻共转运的特征。

Effects of high external concentrations of K+ on 86Rb+ efflux in human platelets: evidence for Na+/K+/2Cl- co-transport.