Salt and water transport across alveolar and distal airway epithelia in the adult lung

Abstract

Substantial progress has been made in understanding the role of the distal airway and alveolar epithelial barriers in regulating lung fluid balance. Molecular, cellular, and whole animal studies have demonstrated that reabsorption of fluid from the distal air spaces of the lung is driven by active sodium transport. Several different in vivo, in situ, and isolated lung preparations have been used to study the mechanisms that regulate fluid transport in the normal and injured lung. Catecholamine-dependent and -independent regulatory mechanisms have been identified that modulate fluid transport, probably by acting on apical sodium channel uptake or the activity of the Na, K-ATPase pumps. Recently, a family of molecular water channels (aquaporins) has been identified that are small (approximately 30 kDa) integral membrane proteins expressed widely in fluid-transporting epithelia and endothelia. At present, four different water channels have been identified in trachea and lung. Measurements of osmotic water permeability in in situ perfused lung and isolated perfused airways suggest a significant contribution of these molecular water channels to measured water permeability. However, further studies are required to determine the role of these water channels in normal pulmonary physiology and disease. Recent studies have provided new insights into the role of the alveolar epithelial barrier in clinical and experimental acute lung injury. Unlike the lung endothelium, the alveolar epithelium is resistant to several clinically relevant types of injury, including endotoxemia and bacteremia as well as aspiration of hyperosmolar solutions. In addition, even when the alveolar barrier has been injured, its capacity to transport edema fluid from the distal air spaces of the lung recovers rapidly. Future studies need to integrate new insights into the molecular mechanisms of alveolar epithelial sodium and water transport with functional studies in the normal and injured lung.

The Aquaporins, Blueprints for Cellular Plumbing Systems

“…Pulmonary tissues develop a large capacity for fluid absorption in the perinatal state and provide humidification of the airways and airway secretions (see Ref. 41 for review). To accomplish this, complex developmental expression patterns have evolved (42) with highly specific distribution patterns (32): AQP1 in peribronchiolar capillary endothelium; AQP3 in basal cells of airway epithelium; AQP4 in tall columnar cells; AQP5 in the apical membrane of type I alveolar pneumocytes and salivary acini.…”

Mild dehydration: a risk factor of broncho-pulmonary disorders?

“…Experimental lung preparations have measured salt and water transport across alveolar and distal airway epithelia. It is generally accepted that the net balance between electrolyte absorption and secretion controls the movement of fluid by osmotic pressure (Boucher, 1994a;Matthay et al, 1996). A primary motion force for the transport of sodium seems to be the sodium/potassium-ATPase (sensitive to oubain), located on the basolateral membrane ( Figure 2).…”

Role of the pulmonary epithelium and inflammatory signals in acute lung injury

“…Water can travel through transcellular channels known as aquaporins. However, studies using specific aquaporin-null mice have demonstrated that these channels do not have significant roles in alveolar fluid absorption despite their importance in osmotically driven water movement across epithelial and endothelial cell barriers in the lung [10][11][12][13][14][15]. Cl − is secreted into the alveolar space via the cystic fibrosis transmembrane regulator (CFTR) [16]; this receptor also plays a role in cAMP-mediated fluid transport [17,18].…”