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• W15671949 abstract "The epithelial Na+ channel (ENaC) is located in the luminal membrane of salt absorbing epithelia such as kidney collecting ducts, airways, colon and glandular excretory ducts. When co-expressed in the same cell, activation of CFTR Cl– channels as well as other Cl– channels inhibit epithelial Na+ channels and thus limit Na+ absorption. Inhibition of ENaC by Cl– conductance has been demonstrated in airways, colonic and kidney epithelial cells and overexpressing recombinant cells, such as Xenopus oocytes. Thus, inhibition of ENaC is not unique to CFTR but is most likely mediated by an increase in intracellular Cl–, at least in Xenopus oocytes and M1 mouse collecting duct cells. Cl–-dependent feedback regulation of ENaC has also been demonstrated previously in mouse mandibular duct cell, however, we were unable to detect a specific Cl– sensitive protein mediating this inhibitory effect on ENaC in Xenopus oocytes. Our data suggest a rather direct interference of Cl– with the epithelial Na+ channel. ENaC is also inhibited by activation of purinergic receptors, as demonstrated in airway epithelial cells and other cell types such as cultured collecting duct cells. The inhibition of ENaC is less pronounced in M1 cells but is prominent in airway epithelia, where a Ca2+ dependent Cl– conductance is activated in parallel to the inhibition of the Na+ conductance. Further experiments demonstrated a Cl– dependence for the purinergic inhibition of ENaC in mouse trachea. Thus both, CFTR and purinergic inhibition of Na+ absorption are Cl– dependent and suggest common downstream mechanisms. In this regard, a Cl– sensitive site is suggested for the epithelial Na+ channel. Cystic Fibrosis is characterized by a loss of the cAMP activated CFTR Cl– conductance and by enhanced Na+ absorption in airways and colon. A primary goal of novel pharmacotherapy is the inhibition of the enhanced Na+ conductance in CF airways. Puringeric stimulation with stabilized ATP or UTP derivatives such as INS365 and thus downregulation of ENaC with parallel activation of Ca2+-dependent Cl– channels should restore Cl– secretion and reduce exaggerated salt absorption. Equally, a better understanding of the Cl–-dependent mechanism of EnaC regulation may identify new therapeutic targets." @default.
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• W15671949 date "2004-01-01" @default.
• W15671949 modified "2023-09-27" @default.
• W15671949 title "Inhibition of epithelial Na+ channels by CFTR and purinergic agonists: Mechanisms and significance for CF" @default.
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