Abstract
This review summarizes the newly discovered molecular mechanism of secretin-stimulated urine HCO3- excretion and the role of cystic fibrosis transmembrane conductance regulator (CFTR) in renal HCO3- excretion. The secretin receptor is functionally expressed in the basolateral membrane of the HCO(3)(-)secreting beta-intercalated cells of the collecting duct. Here it activates a fast and efficient ...
Abstract
This review summarizes the newly discovered molecular mechanism of secretin-stimulated urine HCO3- excretion and the role of cystic fibrosis transmembrane conductance regulator (CFTR) in renal HCO3- excretion. The secretin receptor is functionally expressed in the basolateral membrane of the HCO(3)(-)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 mice and 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.
Altmetric