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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Na+,K+ pump and Na+-coupled ion carriers in isolated mammalian kidney epithelial cells: regulation by protein kinase C.
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Na+,K+ pump and Na+-coupled ion carriers in isolated mammalian kidney epithelial cells: regulation by protein kinase C.

机译：分离的哺乳动物肾上皮细胞中的Na +，K +泵和Na +耦合的离子载体：蛋白激酶C的调控

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摘要

This review updates our current knowledge on the regulation of Na+/H+ exchanger, Na+,K+,Cl- cotransporter, Na+,Pi cotransporter, and Na+,K+ pump in isolated epithelial cells from mammalian kidney by protein kinase C (PKC). In cells derived from different tubule segments, an activator of PKC, 4beta-phorbol 12-myristate 13-acetate (PMA), inhibits apical Na+/H+ exchanger (NHE3), Na+,Pi cotransport, and basolateral Na+,K+ cotransport (NKCCl) and augments Na+,K+ pump. In PMA-treated proximal tubules, activation of Na+,K+ pump probably plays a major role in increased reabsorption of salt and osmotically obliged water. In Madin-Darby canine kidney (MDCK) cells, which are highly abundant with intercalated cells from the collecting duct, PMA completely blocks Na+,K+,Cl- cotransport and decreases the activity of Na+,Pi cotransport by 30-40%. In these cells, agonists of P2 purinoceptors inhibit Na+,K+,Cl- and Na+,Pi cotransport by 50-70% via a PKC-independent pathway. In contrast with MDCK cells, in epithelial cells derived from proximal and distal tubules of the rabbit kidney, Na+,K+,Cl- cotransport is inhibited by PMA but is insensitive to P2 receptor activation. In proximal tubules, PKC-induced inhibition of NHE3 and Na+,Pi cotransporter can be triggered by parathyroid hormone. Both PKC and cAMP signaling contribute to dopaminergic inhibition of NHE3 and Na+,K+ pump. The receptors triggering PKC-mediated activation of Na+,K+ pump remain unknown. Recent data suggest that the PKC signaling system is involved in abnormalities of dopaminergic regulation of renal ion transport in hypertension and in the development of diabetic complications. The physiological and pathophysiological implications of PKC-independent regulation of renal ion transporters by P2 purinoceptors has not yet been examined.
机译：这篇综述更新了我们目前对蛋白激酶C（PKC）对来自哺乳动物肾脏的分离的上皮细胞中Na + / H +交换子，Na +，K +，Cl-协同转运蛋白，Na +，Pi协同转运蛋白和Na +，K +泵的调节的认识。在衍生自不同肾小管节段的细胞中，PKC的活化剂，4β-佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）抑制根尖Na + / H +交换子（NHE3），Na +，Pi共转运和基底外侧Na +，K +共转运（NKCCl）并增加Na +，K +泵。在PMA处理的近端小管中，Na +，K +泵的激活可能在增加盐和渗透性水的重吸收中起主要作用。在Madin-Darby犬肾（MDCK）细胞中，该细胞高度富含来自收集管的插层细胞，PMA完全阻断Na +，K +，Cl-共转运，并使Na +，Pi共转运活性降低30-40％。在这些细胞中，P2嘌呤受体激动剂通过不依赖PKC的途径抑制Na +，K +，Cl-和Na +，Pi共转运50-70％。与MDCK细胞相反，在源自兔肾脏近端和远端小管的上皮细胞中，Na +，K +，Cl-共转运受PMA抑制，但对P2受体激活不敏感。在近端小管中，甲状旁腺激素可触发PKC诱导的NHE3和Na +，Pi共转运蛋白的抑制。 PKC和cAMP信号均有助于NHE3和Na +，K +泵的多巴胺能抑制。触发PKC介导的Na +，K +泵激活的受体仍然未知。最新数据表明，PKC信号系统参与高血压中肾脏离子转运的多巴胺能调节异常和糖尿病并发症的发展。尚未研究过P2嘌呤受体对PKC独立调节肾离子转运蛋白的生理和病理生理影响。

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