We hypothesized that inhibition and activation of basolateral to luminal chloride transport mechanisms were associated with respective decreases and increases in basolateral to luminal water fluxes. The luminal to basolateral (J W L→B ) and basolateral to luminal (J W B→L ) water fluxes across ovine tracheal epithelia were measured simultaneously. The mean J W L→B (6.5 μl/min/cm2) was larger than J W B→L (6.1 μl/min/cm2). Furosemide reduced J W B→L from 6.0 to 5.6 μl/min/cm2. Diphenylamine-2-carboxylate (DPC) reduced J W B→L from 7.9 to 7.3 μl/min/cm2 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 increased J W B→L from 4.9 to 6.0 μl/min/cm2. Neuropeptide Y in the presence of norepinephrine decreased J W L→B (6.4 to 5.2 μl/min/cm2) and returned J W B→L to its baseline value. Vasopressin increased J W B→L from 4.1 to 5.1 μl/min/cm2. Endothelin-1 induced a simultaneous increase in J W B→L (7.0 to 7.7 μl/min/cm2) and decrease in J W L→B (7.4 to 6.4 μl/min/cm2); and decreased the membrane resistance. These data indicate that in tracheal epithelia under homeostatic conditions J W B→L has a ∼15% actively coupled component. Consistent with our hypothesis, inhibition and receptor-induced stimulation of chloride effluxes were associated with decreases and increases in J W B→L , respectively. However, as inhibition of transcellular chloride transport always decreased J W L→B more than J W B→L , reducing transepithelial chloride transport did not result in less water being transported into the airway lumen.
The Journal of Membrane Biology – Springer Journals
Published: Jun 1, 2000
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