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Autor(en) / Beteiligte
Titel
121 THE CALCIUM-INDEPENDENT COMPONENT OF THE SHUNT PATHWAY IN RABBIT ESOPHAGEAL EPITHELIUM
Ist Teil von
  • Journal of investigative medicine, 2005-01, Vol.53 (1), p.S274-S274
Ort / Verlag
London: Sage Publications Ltd
Erscheinungsjahr
2005
Link zum Volltext
Quelle
Alma/SFX Local Collection
Beschreibungen/Notizen
  • Aim/BackgroundWe previously reported that exposure of rabbit esophageal epithelium (EE) in Ussing chambers to calcium-free solution reduces the transepithelial electrical resistance (RT), progressively over 2 hours by ˜ 35%. RT declines over the next 2 hours by ˜ 10% to reach a plateau. Since shunt pathway resistance dominates RT, the limited decline observed in RT indicates that ˜ 50% of the shunt pathway consists of a calcium-independent component.MethodsTo further examine the calcium-independent component of RT, rabbit EE was mounted in Ussing chambers and exposed luminally to either of two environments previously shown to reduce RT to a similar degree as calcium-free solution: 1) hypertonic urea, 0.5 M, and 2) HCl, pH 1.6.Results(Means ± SEM, n ≥ 4). The addition of luminal urea, but not HCl, to a calcium-free solution for 1 hour resulted in a marked decline in RT (41 ± 4%) to a value well below that produced by continued calcium-free alone (reduced 22 ± 3%). These data indicating that hypertonic urea alters the shunt pathway in a fashion that is distinct from calcium-free solution are also supported by 2 sets of experiments in which the flux of fluorescein, 300 mol. wt., in calcium-free solution plus urea was increased 2-3 fold over that of calcium-free solution alone.ConclusionsThe shunt pathway in rabbit esophageal epithelium is composed of two components, one calcium dependent and the other calcium independent. The calcium-independent component is sensitive to luminal hypertonic urea but not HCl. This sensitivity suggests that other structures, possibly the close apposition of adjacent cell membranes surrounding the intercellular space, contribute in important ways to the barrier function of EE. Support: NIH DK36013.
Sprache
Englisch
Identifikatoren
ISSN: 1081-5589
eISSN: 1708-8267
DOI: 10.2310/6650.2005.00006.120
Titel-ID: cdi_proquest_journals_1786934144
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