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Regulation of renal Na-(K)-Cl cotransporters by vasopressin

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Abstract

Vasopressin (AVP) induces antidiuresis, thus playing an essential role in body water and electrolyte homeostasis. Its antidiuretic effects are mediated chiefly by V2 vasopressin receptors (V2R) expressed along the distal nephron and collecting duct epithelia. NaCl reabsorption in the distal nephron, which includes the thick ascending limb (TAL) and distal convoluted tubule (DCT), largely depends on the activity of two structurally related Na-(K)-Cl cotransporters, NKCC2 in TAL and NCC in DCT. AVP-induced activation of these transporters contributes to urine concentration and renal electrolyte reabsorption. Previous work has specified molecular pathways mediating the effects of V2R activation in TAL and DCT, and protein networks involved in intracellular trafficking and phosphoregulation of the two transporters have been identified. This review summarizes recent progress in understanding AVP signalling mechanisms that are responsible for the activation of NKCC2 and NCC. Implications in the pathophysiology of diseases such as nephrogenic diabetes insipidus, diabetes mellitus and salt-sensitive hypertension are discussed in this context.

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Acknowledgements

We would like to acknowledge Martin Thomson and Torsten Giesecke for constructive discussions and technical help.

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Correspondence to Kerim Mutig.

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The present study was supported by grants from the Deutsche Forschungsgemeinschaft (DFG: MU 2924/2-2 and BA 700/22-2).

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The authors declare that they have no conflicts of interest.

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This article is part of the special issue on Functional Anatomy of the Kidney in Health and Disease in Pflügers Archiv – European Journal of Physiology

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Bachmann, S., Mutig, K. Regulation of renal Na-(K)-Cl cotransporters by vasopressin. Pflugers Arch - Eur J Physiol 469, 889–897 (2017). https://doi.org/10.1007/s00424-017-2002-2

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  • DOI: https://doi.org/10.1007/s00424-017-2002-2

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