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The molecular mechanism of CFTR- and secretin-dependent renal bicarbonate excretion

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This review summarizes the newly discovered molecular mechanism of secretin-stimulated urine HCO3- excretion and the role of CFTR in renal HCO3- excretion. The secretin receptor is functionally expressed in the basolateral membrane of the HCO3- secreting beta-intercalated cells of the collecting duct. Here it activates a fast and efficient secretion of HCO3- into the urine serving to normalize metabolic alkalosis. The ability to acutely increase renal base excretion is entirely dependent on functional pendrin (SLC26A4) and CFTR, and both proteins localize to the apical membrane of the beta-intercalated cells. In cystic fibrosis (CF) mice and also in CF patients, this function is absent or markedly reduced. We discuss that the alkaline tide, namely the transient urine alkalinity after a meal, has now received a clear physiological explanation. This article is protected by copyright. All rights reserved
Original languageEnglish
JournalThe Journal of Physiology
Publication statusE-pub ahead of print - May 2021

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