The lungs of the fetus are filled with fluid and it is essential that fetal lung fluid is
cleared at birth. This process is mediated through the activation of airway epithelial sodium
channels (ENaC). In animals, ENaC is considered crucial for postnatal pulmonary adaptation.
In humans, postnatal ENaC expression is dependent on gestational age and its activity,
measured as nasal potential difference, correlates with lung compliance. Therefore, in the
human newborn infant ENaC may be important for physiologic postnatal adaptation. The activity
of ENaC is increased by beta-agonists, such as salbutamol. We hypothesize that low pulmonary
expression or activity of ENaC in the perinatal period causes delayed clearance of lung fluid
and thereby contributes to the risk for development of transient tachypnea of the newborn
(TTN) in term infants born by Caesarean section (CS).