Actions of Hydrogen Sulfide on Sodium Transport Processes across Native Distal Lung Epithelia (Xenopus laevis)

Hydrogen sulfide (H(2)S) is well known as a highly toxic environmental chemical threat. Prolonged exposure to H(2)S can lead to the formation of pulmonary edema. However, the mechanisms of how H(2)S facilitates edema formation are poorly understood. Since edema formation can be enhanced by an impaired clearance of electrolytes and, consequently, fluid across the alveolar epithelium, it was questioned whether H(2)S may interfere with transepithelial electrolyte absorption. Electrolyte absorption was electrophysiologically measured across native distal lung preparations (Xenopus laevis) in Ussing chambers. The exposure of lung epithelia to H(2)S decreased net transepithelial electrolyte absorption. This was due to an impairment of amiloride-sensitive sodium transport. H(2)S inhibited the activity of the Na(+)/K(+)-ATPase as well as lidocaine-sensitive potassium channels located in the basolateral membrane of the epithelium. Inhibition of these transport molecules diminishes the electrochemical gradient which is necessary for transepithelial sodium absorption. Since sodium absorption osmotically facilitates alveolar fluid clearance, interference of H(2)S with the epithelial transport machinery provides a mechanism which enhances edema formation in H(2)S-exposed lungs.