title: 5-Hydroxytryptamine inhibits Na absorption and stimulates Cl secretion across canine tracheal epithelial sheets.
abstract: BACKGROUND
  5-Hydroxytryptamine (5-HT) can be released from mast cells and platelets through an IgE-dependent mechanism and may play a role in the pathogenesis of allergic bronchoconstriction. However, the effect of 5-HT on ion transport by airway epithelium remains uncertain.
  
  
  OBJECTIVE
  To determine whether 5-HT alters electrical and ion transport properties of Cl-secreting epithelia and, if so, what subtype of 5-HT receptors is involved, we studied canine tracheal epithelium under short-circuit conditions in vitro.
  
  
  METHODS
  Canine tracheal mucosa was mounted in Lucite half-chambers and the responses of short-circuit current (lsc), transepithelial potential difference (PD) and tissue conductance (G) were measured. In addition, ion fluxes were directly measured using 22Na and 36Cl.
  
  
  RESULTS
  Mucosal addition of 5-HT caused a rapid increase in lsc, which was accompanied by the increases in PD and G, whereas submucosal 5-HT had no effect. In the presence of amiloride, 5-HT and its receptor agonists dose-dependently increased lsc, with the rank order of potency being 5-HT > alpha-methyl-5-HT > 2-methyl-5HT > 5-carboxamidotryptamine. The effect of 5-HT was inhibited by ketanserin and spiperone but not by ondansetron. 5-HT increased Cl flux from the submucosa to the mucosa with a slight inhibition of Na flux to the opposite direction.
  
  
  CONCLUSIONS
  5-HT inhibits airway epithelial Na absorption and stimulates Cl secretion. The latter action predominates the former and is mediated by 5-HT2 receptors. These effects may result in the increase in water movement toward the airway lumen.
authors.affiliation: First Department of Medicine, Tokyo Women's Medical College, Japan.
authors.forename: J
authors.initials: J
authors.lastname: Tamaoki
authors.forename: A
authors.initials: A
authors.lastname: Chiyotani
authors.forename: H
authors.initials: H
authors.lastname: Takemura
authors.forename: K
authors.initials: K
authors.lastname: Konno
mesh_terms: D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D018118:Chloride Channels / Q000187:drug effects; D002713:Chlorine / Q000378:metabolism*; D004232:Diuretics / Q000494:pharmacology; D004285:Dogs; D018492:Dopamine Antagonists / Q000494:pharmacology; D004553:Electric Conductivity; D004558:Electric Stimulation; D004848:Epithelium / Q000187:drug effects / Q000378:metabolism; D005260:Female; D066298:In Vitro Techniques; D015640:Ion Channel Gating / Q000187:drug effects / Q000502:physiology; D007650:Ketanserin / Q000494:pharmacology; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D017294:Ondansetron / Q000494:pharmacology; D012701:Serotonin / Q000494:pharmacology*; D012702:Serotonin Antagonists / Q000494:pharmacology; D012964:Sodium / Q000037:antagonists & inhibitors* / Q000493:pharmacokinetics*; D015222:Sodium Channels / Q000187:drug effects; D013134:Spiperone / Q000494:pharmacology; D014132:Trachea / Q000187:drug effects* / Q000502:physiology*
chemical_list: D018118:Chloride Channels; D004232:Diuretics; D018492:Dopamine Antagonists; D012702:Serotonin Antagonists; D015222:Sodium Channels; D012701:Serotonin; D017294:Ondansetron; D002713:Chlorine; D013134:Spiperone; D000584:Amiloride; D007650:Ketanserin; D012964:Sodium