An infant born by cesarean delivery is at risk of having excessive pulmonary fluid which makes predisposition to transient tachypnea of the newborn (TTN), because fetal thorax compression during labor leads to the loss of large volumes liquid from the lungs. At birth, the pulmonary epithelium switches from predominantly facilitated Cl⁻ secretion to predominantly active Na+ reabsorption with the increase expression epithelial Na+ -channels (ENaC). Diminished activity or immaturity of this process may contribute to the development of TTN. Familial clustering of some TTN cases shows a genetic predisposition in the developing of this disorder. Antenatal glucocorticoids induce lung Na+ reabsorption by increasing the number and activity of channels even in hypoxia. Since a large release of fetal adrenaline occurs late in labor stimulating ENaC to start reabsorbing lung fluids, aerolized ß-agonists may be used in the treatment. Genetic predisposition for ß-adrenergic hyporesponsiveness may cause TTN in newborn period, and asthma/wheezing in older age groups. Although furosemide accelerates lung fluid resorption and cause pulmonary vasodilatation, oral or aerosolized furosemide cannot be recommended as treatment for TTN unless additional data become available.