Impact of mechanical stress on ion transport in native lung epithelium (Xenopus laevis): short-term activation of Na+, Cl (-) and K+ channels.
Epithelia, in general, and the lung epithelium, in particular, are exposed to mechanical forces, but little is known about their impact on pulmonary ion transport. In our present study, we employed transepithelial ion transport measurements on Xenopus lung preparations using custom-built Ussing chambers. Tissues were exposed to mechanical stress by increasing the water column (5 cm) at one side of the tissues. Apical exposure to hydrostatic pressure significantly decreased the short circuit current (I (SC): 24 +/- 1%, n = 152), slightly decreased the transepithelial resistance (R (T): 7 +/- 2%, n = 152), but increased the apical membrane capacitance (C (M): 16 +/- 6%, n = 9). The pressure-induced effect was sensitive to Na+ (amiloride), Cl(-) (DIDS, NFA, NPPB) and K+ channel blockers (Ba2+), glibenclamide). Further on, it was accompanied by increased extracellular ATP levels. The results show that mechanical stress leads to an activation of Na+, Cl(-), and K+ conductances in a native pulmonary epithelium resulting in a net decrease of ion absorption. This could be of considerable interest, since an altered ion transport may contribute to pathophysiological conditions, e.g., the formation of pulmonary edema during artificial ventilation.
Bogdan
Roman
R
Institute of Animal Physiology, Justus-Liebig University Giessen, Wartweg 95, 35392, Giessen, Germany.
Veith
Christine
C
Clauss
Wolfgang
W
Fronius
Martin
M
D000255:Adenosine Triphosphate / Q000502:physiology; D000465:Algorithms; D000818:Animals; D018118:Chloride Channels / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000502:physiology*; D015194:Diffusion Chambers, Culture; D004848:Epithelium / Q000502:physiology*; D005260:Female; D006874:Hydrostatic Pressure; D066298:In Vitro Techniques; D007473:Ion Channels / Q000502:physiology*; D008168:Lung / Q000502:physiology*; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000378:metabolism / Q000502:physiology*; D026941:Sodium Channel Blockers / Q000494:pharmacology; D015222:Sodium Channels / Q000378:metabolism / Q000502:physiology*; D013314:Stress, Mechanical; D014982:Xenopus laevis
D018118:Chloride Channels; D007473:Ion Channels; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D026941:Sodium Channel Blockers; D015222:Sodium Channels; D000255:Adenosine Triphosphate