title: Bidirectional transepithelial water transport: chloride-dependent mechanisms.
abstract: 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 microl/min/cm(2)) was larger than J(W)(B-->L) (6.1 microl/min/cm(2)). Furosemide reduced J(W)(B-->L) from 6.0 to 5.6 microl/min/cm(2). Diphenylamine-2-carboxylate (DPC) reduced J(W)(B-->L) from 7.9 to 7. 3 microl/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 increased J(W)(B-->L) from 4.9 to 6.0 microl/min/cm(2). Neuropeptide Y in the presence of norepinephrine decreased J(W)(L-->B) (6.4 to 5.2 microl/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 microl/min/cm(2). Endothelin-1 induced a simultaneous increase in J(W)(B-->L) (7.0 to 7.7 microl/min/cm(2)) and decrease in J(W)(L-->B) (7.4 to 6.4 microl/min/cm(2)); and decreased the membrane resistance. These data indicate that in tracheal epithelia under homeostatic conditions J(W)(B-->L) has a approximately 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.
authors.affiliation: Department of Medicine, University of Illinois at Chicago, 1940 W. Taylor Street, Chicago, IL 60612, USA.
authors.forename: J E
authors.initials: JE
authors.lastname: Phillips
authors.forename: D B
authors.initials: DB
authors.lastname: Yeates
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000818:Animals; D001692:Biological Transport; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002712:Chlorides / Q000378:metabolism*; D019332:Endothelin-1 / Q000494:pharmacology; D005665:Furosemide / Q000494:pharmacology; D066298:In Vitro Techniques; D009478:Neuropeptide Y / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D020545:Respiratory Mucosa / Q000187:drug effects / Q000378:metabolism; D012756:Sheep; D014132:Trachea / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D014667:Vasopressins / Q000494:pharmacology; D014867:Water / Q000378:metabolism*; D062367:ortho-Aminobenzoates / Q000494:pharmacology
chemical_list: D000316:Adrenergic alpha-Agonists; D002121:Calcium Channel Blockers; D002712:Chlorides; D019332:Endothelin-1; D009478:Neuropeptide Y; D062367:ortho-Aminobenzoates; D014867:Water; D014667:Vasopressins; D005665:Furosemide; C001209:fenamic acid; D009638:Norepinephrine