Question: 

Hydrogen sulphide (H₂S) is well known as a toxic gas, but is also endogenously generated in organisms and has recently been identified as a novel physiological signalling mediator. Since it is known that H₂S can interact with a variety of ion channels, we questioned if H₂S might regulate ion transport processes in the pulmonary epithelium.

Methodology: 

Transepithelial ion transport was measured as short-circuit current signals (I_SC) across native lung preparations of Xenopus laevis in Ussing-chambers. H₂S was applied by the donor molecule NaHS.

Results: 

The application of NaHS (1 mM) decreased I_SC by 50%. There was no effect of NaHS on niflumic-acid-sensitive chloride secretion, whereas amiloride-sensitive sodium absorption was significantly decreased. On apically permeabilised epithelia, NaHS inhibited ouabain-sensitive Na⁺/K⁺-ATPase currents. Further, NaHS decreased lidocaine-sensitive potassium currents across functionally isolated basolateral membranes, which were exposed to a potassium gradient in the presence of ouabain.

Conclusion: 

These data indicate that H₂S inhibits amiloride-sensitive sodium absorption across Xenopus lung epithelia. This is likely due to an inhibition of both Na⁺/K⁺-ATPase and potassium channel activity in the basolateral membrane. An impairment of both transporting systems will eventually decrease the electrochemical driving force, which maintains transepithelial sodium absorption. Taken together, H₂S might thus represent a novel regulator of ion transport processes in lung epithelia. Supported by DFG AL 1453/ 1-1.