Going with the flow: New insights regarding flow induced K + secretion in the distal nephron.

Autor: Lasaad S; Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, New York, USA., Nickerson AJ; Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA., Crambert G; Centre de Recherche Des Cordeliers, Institut National de la Santé et de la Recherche Scientifique (INSERM), Sorbonne Université, Université Paris Cité, Laboratoire de Physiologie Rénale et Tubulopathies, Paris, France.; Unité Métabolisme et Physiologie Rénale, Centre National de la Recherche Scientifique (CNRS) EMR 8228, Paris, France., Satlin LM; Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, New York, USA., Kleyman TR; Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.; Department of Cell Biology and Department of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Jazyk: angličtina
Zdroj: Physiological reports [Physiol Rep] 2024 Oct; Vol. 12 (20), pp. e70087.
DOI: 10.14814/phy2.70087
Abstrakt: K + secretion in the distal nephron has a critical role in K + homeostasis and is the primary route by which K + is lost from the body. Renal K + secretion is enhanced by increases in dietary K + intake and by increases in tubular flow rate in the distal nephron. This review addresses new and important insights regarding the mechanisms underlying flow-induced K + secretion (FIKS). While basal K + secretion in the distal nephron is mediated by renal outer medullary K + (ROMK) channels in principal cells (PCs), FIKS is mediated by large conductance, Ca 2+ /stretch activated K + (BK) channels in intercalated cells (ICs), a distinct cell type. BK channel activation requires an increase in intracellular Ca 2+ concentration ([Ca 2+ ] i ), and both PCs and ICs exhibit increases in [Ca 2+ ] i in response to increases in tubular fluid flow rate, associated with an increase in tubular diameter. PIEZO1, a mechanosensitive, nonselective cation channel, is expressed in the basolateral membranes of PCs and ICs, where it functions as a mechanosensor. The loss of flow-induced [Ca 2+ ] i transients in ICs and BK channel-mediated FIKS in microperfused collecting ducts isolated from mice with IC-specific deletion of Piezo1 in the CCD underscores the importance of PIEZO1 in the renal regulation of K + transport.
(© 2024 The Author(s). Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.)
Databáze: MEDLINE
Externí odkaz:
Nepřihlášeným uživatelům se plný text nezobrazuje