Lung epithelial ion transport in neonatal lung disease

Lung epithelial ion transport promotes salt and water movement across the f etal and neonatal lung epithelium. The mechanism is dependent on basolatera l membrane Na-K-ATPase and the apical membrane Cl- and Na+ channels. During fetal life active secretion of Cl- and parallel movement of Na+ across the epithelium into the developing lung lumen induce accumulation of liquid in to the future airspaces. Postnatally, however, absorption of fluid from the airspaces must start. Present evidence suggests that activation of Naf tra nsport from the lumen into the basolateral direction drives fluid absorptio n and results in an essentially dry air-filled alveolus. In laboratory anim als amiloride, a Na+ channel blocker, induces respiratory distress and impe des lung fluid clearance. One of the epithelial amiloride-sensitive Na+ cha nnels, ENaC, is composed of th ree homologous subunits that differentially respond to glucocorticoid hormone. In newborn infants an increase in pulmon ary fluid and a defective Na+ transport associate with respiratory distress . The ontogeny, subunit composition and function of ENaC along the respirat ory tract are currently under investigation. It will be interesting to find out whether the subunit composition and function of lung ENaC respond to t he therapy of the critically ill newborn infant. Copyright (C) 2001 S. Karg er AG, Basel.