title: Electrophysiological basis of human fallopian tubal fluid formation.
abstract: A preparation for the maintenance of human Fallopian tubal epithelial cells as a polarized layer in primary culture was used to study the electrophysiological basis of tubal fluid formation in terms of the movement of Na+, K+ and Cl- ions. Transepithelial potential difference (PD) and short-circuit current (Iscc) were recorded by mounting the epithelial cells in a modified Ussing chamber. Resistance (R) was calculated from the measurements of PD and Iscc. The epithelia, although confluent, formed a 'leaky' electrical system and resistances greater than 300 omega cm-2 were rarely achieved. The sodium channel blocker, amiloride (100 mumol l-1), produced only small effects on PD and Iscc. The potassium channel blocker, tetraethylammonium chloride (TEA) (25 mmol l-1), also produced small, but significant changes in PD, Iscc and R while the chloride channel blocker, 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS) (1 mmol l-1), induced a marked increase in PD and Iscc, and a fall in R, when added to the basal surface of the cells. Bathing the apical surface of the cells with chloride-free medium also produced a marked increase in PD, Iscc and R: bathing the basal surface of the cells with chloride-free medium produced a marked decrease in PD and Iscc. Extracellular ATP (10 mumol l-1), added to either the apical or the basal surface of the cells, induced a transient increase in PD and Iscc and a decrease in R. Amiloride, TEA or furosemide had no effect on the response of the cells to ATP. SITS, applied to the apical surface, significantly reduced the response of the cells to ATP. We conclude that the major driving force for human tubal fluid formation is the transepithelial secretion of chloride ions into the oviduct lumen and that exogenous ATP is a potential modulator of secretion.
authors.affiliation: Department of Biology, University of York, UK.
authors.forename: S J
authors.initials: SJ
authors.lastname: Downing
authors.forename: S D
authors.initials: SD
authors.lastname: Maguiness
authors.forename: A
authors.initials: A
authors.lastname: Watson
authors.forename: H J
authors.initials: HJ
authors.lastname: Leese
mesh_terms: D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000378:metabolism / Q000494:pharmacology; D000584:Amiloride / Q000494:pharmacology; D001826:Body Fluids / Q000502:physiology*; D002352:Carrier Proteins / Q000037:antagonists & inhibitors; D002478:Cells, Cultured; D018118:Chloride Channels / Q000037:antagonists & inhibitors; D002712:Chlorides / Q000378:metabolism; D004594:Electrophysiology; D004848:Epithelium / Q000502:physiology; D005187:Fallopian Tubes / Q000502:physiology*; D005260:Female; D005665:Furosemide / Q000494:pharmacology; D006801:Humans; D017136:Ion Transport / Q000187:drug effects / Q000502:physiology; D011188:Potassium / Q000378:metabolism; D026902:Potassium Channel Blockers; D012964:Sodium / Q000378:metabolism; D026941:Sodium Channel Blockers; D028021:Sodium-Potassium-Chloride Symporters; D019789:Tetraethylammonium / Q000494:pharmacology
chemical_list: D002352:Carrier Proteins; D018118:Chloride Channels; D002712:Chlorides; D026902:Potassium Channel Blockers; D026941:Sodium Channel Blockers; D028021:Sodium-Potassium-Chloride Symporters; D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid; D019789:Tetraethylammonium; D000584:Amiloride; D005665:Furosemide; D000255:Adenosine Triphosphate; D012964:Sodium; D011188:Potassium