layer in CF airways. Consequently,mucus mpactions form, resulting in an impaired mucociliary clearance and subseq predisposition towards bacterial infections By contrast, it is has long been known that CF s associated with a reducti reabsorption within the sweat gland lumen sweatin individuals with CF and provides a characteristic diagnostic feature for CF. To some extent this can be accounted for by the reduction in Cl conductance of the However,计 has been suggested9 expected to decrease the electrochemical driving force for sodium to enter the cell and thereby leads to the secretion fluid containing a much higher content reabsorb sodium is due not only to the electrochemical effects arising from the primary loss of chloride conductance through the CFtR but also to a secondary inability to activate sodium-channel conductance It may therefore be possible that both the activation and inhibition of ENac are governed by CF TR under different circumstances .As you may imagine, in these diseases a global electrolyte imbalance occurs since the homeostasis of other electrolytes also depend in that of Naand Cl, therefore resulting affected as welllayer in CF airways. Consequently, mucus impactions form, resulting in an impaired mucociliary clearance and subsequent predisposition towards bacterial infections. By contrast, it is has long been known that CF is associated with a reduction in sodium reabsorption within the sweat gland lumen. This accounts for the presence of 'salty sweat' in individuals with CF and provides a characteristic diagnostic feature for CF. To some extent this can be accounted for by the reduction in Cl- conductance of the apical membrane of the epithelial cell. This is expected to decrease the electrochemical driving force for sodium to enter the cell and thereby leads to the secretion of fluid containing a much higher content of sodium. However, it has been suggested that failure to reabsorb sodium is due not only to the electrochemical effects arising from the primary loss of chloride conductance through the CFTR but also to a secondary inability to activate sodium-channel conductance. It may therefore be possible that both the activation and inhibition of ENaC are governed by CFTR under different circumstances. ..As you may imagine, in these diseases a global electrolyte imbalance occurs since the homeostasis of other electrolytes also depend in that of Na+ and Cl- , therefore resulting affected as well