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通过皮质集合管顶端钾通道的钾分泌视图。

View of K+ secretion through the apical K channel of cortical collecting duct.

作者信息

Wang W H

机构信息

Department of Pharmacology, New York Medical College, Valhalla, USA.

出版信息

Kidney Int. 1995 Oct;48(4):1024-30. doi: 10.1038/ki.1995.385.

Abstract

The apical small-conductance K+ channel plays an important role in renal K+ secretion, as evidenced by the presence of the extensive modulatory pathways. Figure 3 summarizes the current understanding of the mechanisms that modulate the apical small-conductance K+ channel. Stimulation of adenylate cyclase enhances channel activity and consequently K+ secretion. In contrast, increases in intracellular Ca2+ concentration and activation of Ca(2+)-dependent signal transduction pathways inhibit the K+ channel and thus decrease K+ secretion. The vasopressin-induced stimulation of K+ secretion in CCD results at least in part from cAMP-dependent signal transduction pathways. The Ca(2+)-dependent signal transduction pathway is responsible for modulatory coupling between Na+ pump turnover and apical K+ conductance when the Na+ pump is inhibited.

摘要

顶端小电导钾通道在肾脏钾分泌中起重要作用,广泛的调节途径的存在证明了这一点。图3总结了目前对调节顶端小电导钾通道机制的理解。腺苷酸环化酶的刺激增强通道活性,从而促进钾分泌。相反,细胞内钙离子浓度的增加和钙依赖信号转导途径的激活抑制钾通道,从而减少钾分泌。抗利尿激素诱导的皮质集合管钾分泌刺激至少部分源于cAMP依赖的信号转导途径。当钠泵受到抑制时,钙依赖信号转导途径负责钠泵周转与顶端钾电导之间的调节偶联。

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