Calonge M L, Cano M, Ilundáin A A
Departamento Fisiología y Biología Animal, Facultad de Farmacia, Universidad de Sevilla, Spain.
Exp Physiol. 1998 Sep;83(5):629-38. doi: 10.1113/expphysiol.1998.sp004144.
Potassium transport was measured in isolated chicken colonocytes using 85Rb+ as a tracer for K+. Rb+ was determined by atomic absorption spectrometry. The results revealed that net K+ uptake occurred via at least four mechanisms: (i) Na+,K(+)-ATPase, (ii) K(+)-ATPase, (iii) Na(+)-K(+)-2Cl- cotransport system and (iv) a mechanism(s) which is resistant to both ouabain and bumetanide. The rate of K+(Rb+) efflux is stimulated by the calcium ionophore A23187, inhibited by either quinine, verapamil or Ba2+, and unaffected by either apamin, 3,4-diaminopyridine (3,4-DAP), H2-DIDS or bumetanide. The A23187-induced increase in K+(Rb+) efflux was abolished by apamin. These findings suggest that K+(Rb+) efflux from chicken colonocytes occurs at least in part through Ca(2+)-activated K+ channels. The present results also show that all these K+ transport systems are involved in cell volume regulation. Thus, external hyposmolarity decreased net K+(Rb+) uptake mediated by Na+,K(+)-ATPase, K(+)-ATPase and the Na(+)-K(+)-2Cl- cotransporter and increased K+(Rb+) efflux rate. The opposite was observed under hyperosmotic conditions.
利用⁸⁵Rb⁺作为K⁺的示踪剂,在分离的鸡结肠细胞中测量钾转运。通过原子吸收光谱法测定Rb⁺。结果显示,净K⁺摄取至少通过四种机制发生:(i) Na⁺,K⁺-ATP酶,(ii) K⁺-ATP酶,(iii) Na⁺-K⁺-2Cl⁻协同转运系统,以及(iv) 一种对哇巴因和布美他尼均有抗性的机制。K⁺(Rb⁺)外流速率受钙离子载体A23187刺激,受奎宁、维拉帕米或Ba²⁺抑制,不受蜂毒明肽、3,4-二氨基吡啶(3,4-DAP)、H2-DIDS或布美他尼影响。蜂毒明肽消除了A23187诱导的K⁺(Rb⁺)外流增加。这些发现表明,鸡结肠细胞的K⁺(Rb⁺)外流至少部分通过Ca²⁺激活的K⁺通道发生。目前的结果还表明,所有这些K⁺转运系统都参与细胞体积调节。因此,细胞外低渗降低了由Na⁺,K⁺-ATP酶、K⁺-ATP酶和Na⁺-K⁺-2Cl⁻共转运体介导的净K⁺(Rb⁺)摄取,并增加了K⁺(Rb⁺)外流速率。在高渗条件下观察到相反的情况。