Bidirectional transepithelial water transport: Chloride-dependent mechanisms

We hypothesized that inhibition and activation of basolateral to luminal ch loride transport mechanisms were associated with respective decreases and i ncreases in basolateral to luminal water fluxes. The luminal to basolateral (J(W)(L-->B)) and basolateral lo luminal (J(W)(B-->L)) water fluxes across ovine tracheal epithelia were measured simultaneously. The mean J(W)(L-->B ) (6.5 mu l/min/cm(2)) was larger than J(W)(B-->L) (6.1 mu l/min/cm(2)). Fu rosemide reduced J(W)(B-->L) from 6.0 to 5.6 mu l/min/cm(2). Diphenylamine- 2-carboxylate (DPC) reduced J(W)(B-->L) from 7.9 to 7.3 mu l/min/cm(2) and reduced the membrane potential difference by 38%. Furosemide together with DPC decreased J(W)(L-->B) by 30% and J(W)(B-->L) by 15%, Norepinephrine inc reased J(W)(B-->L) from 4.9 to 6.0 mu l/min/cm(2). Neuropeptide Y in the pr esence of norepinephrine decreased J(W)(L-->B) (6.4 to 5.2 mu l/min/cm(2)) and returned J(W)(B-->L) to its baseline value. Vasopressin increased J(W)( B-->L) from 4.1 to 5.1 mu l/min/cm(2). Endothelin-1 induced a simultaneous increase in J(W)(B-->L) (7.0 to 7.7 mu l/min/cm(2)) and decrease in J(W)(L- ->B) (7.4 to 6.4 mu l/min/cm(2)); and decreased the membrane resistance. Th ese data indicate that in tracheal epithelia under homeostatic conditions J (W)(B-->L) has a similar to 15% actively coupled component. Consistent with our hypothesis, inhibition and receptor-induced stimulation of chloride ef fluxes were associated with decreases acid increases in J(W)(B-->L), respec tively. However, as inhibition of transcellular chloride transport always d ecreased J(W)(L-->B) more than J(W)(B-->L), reducing transepithelial chlori de transport did not result in less water being transported into the airway lumen.