European Respiratory Society

Figure 2

Fri, 2021-07-09 15:57 -- admin
Cellular models of electrolyte secretion: secretory pathway. In airway cells, under conditions triggering secretion, Cl- is taken up from the basolateral (blood) side by the Na+/K+/2Cl- cotransporter. K+ recycles through basolateral K+ channels. This leads to basolateral membrane hyperpolarisation, which, in turn, electrically drives Cl- to the luminal side of the epithelium and stimulates Cl- secretion through the cystic fibrosis transmembrane conductance regulator (CFTR) and/or calcium-activated chloride channels (CaCCs). Activation of the A2B adenosine receptor results in raised cell cyclic adenosine monosphosphate (cAMP) levels, which, in turn, activate the CFTR sufficiently to provide CFTR-dependent regulation of the epithelial sodium channel (ENaC) and Cl- secretion, together with activation of the cAMP-dependent potassium channel (KV7.1). Higher ATP concentrations activate the P2Y2 P2Y receptor, inhibiting Na+ absorption and activating both CFTR-dependent and CFTR-independent Cl- secretion, the latter mediated by the release of cytoplasmic Ca2+, which, in turn, activates the CaCC and the calcium-activated potassium channel (KCa3.1). Na+ is pumped out of the cell by sodium–potassium adenosine triphosphatase (Na+,K+-ATPase). Na+ is secreted via the paracellular shunt following the electrical driving force generated by the negative transepithelial voltage in the lumen. ATP: adenosine triphosphate; UTP: uridine triphosphate; PKA: protein kinase A. ↑: increased; -: inhibition.
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<atom:contributor xmlns:atom="" xmlns:hwp="" xmlns:nlm="" hwp:inherited="yes" nlm:contrib-type="author"><atom:name>I. Fajac</atom:name><nlm:name name-style="western" hwp:sortable="Fajac I."><nlm:surname>Fajac</nlm:surname><nlm:given-names>I.</nlm:given-names></nlm:name></atom:contributor>
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