Regulation of Sodium Transport in A6 Epithelia by Prostaglandin E(2)
Paunescu, Teodor Gabriel
This item is only available for download by members of the University of Illinois community. Students, faculty, and staff at the U of I may log in with your NetID and password to view the item. If you are trying to access an Illinois-restricted dissertation or thesis, you can request a copy through your library's Inter-Library Loan office or purchase a copy directly from ProQuest.
Permalink
https://hdl.handle.net/2142/85493
Description
Title
Regulation of Sodium Transport in A6 Epithelia by Prostaglandin E(2)
Author(s)
Paunescu, Teodor Gabriel
Issue Date
1999
Doctoral Committee Chair(s)
Helman, Sandy I.
Department of Study
Biophysics and Computational Biology
Discipline
Biophysics and Computational Biology
Degree Granting Institution
University of Illinois at Urbana-Champaign
Degree Name
Ph.D.
Degree Level
Dissertation
Keyword(s)
Biophysics, Medical
Language
eng
Abstract
A pulse method of blocker-induced noise analysis was used to study the time-dependent changes of channel density (NT), channel open probability (Po) and single-channel current (iNa) of apical membrane epithelial Na + channels (ENaCs) in A6 epithelia in response to 1 muM PGE 2 added to the basolateral solution. Epithelia were investigated in both unstimulated (n = 11) and aldosterone-stimulated states of Na + transport (n = 8) where changes of transport measured as amiloride-sensitive short-circuit currents (INa) could be decomposed into the underlying time-dependent changes of iNa, Po and NT. After a short delay of about 1 min, INa increased to maximum values within approximately 17 min (6.4 +/- 0.6 to 16.5 +/- 1.0 muA/cm 2 in unstimulated tissues; 18.0 +/- 1.7 to 26.5 +/- 2.1 muA/cm 2 in aldosterone-stimulated tissues). Increases of transport and decreases of single-channel current from mean values of 0.40 +/- 0.01 to 0.24 +/- 0.02 pA in unstimulated tissues and from 0.37 +/- 0.01 to 0.23 +/- 0.02 pA in aldosterone-stimulated tissues mandated mean increases of open channel density No = P oNT of 355 +/- 44% and 161 +/- 28% in unstimulated and aldosterone-stimulated tissues, respectively, at 17 min following PGE2 treatment. The increases of open channel density from baseline values of 18.4 +/- 1.4 (unstimulated) and 52.9 +/- 4.5 (aldosterone-stimulated) channels/100mum2 were due to increases of the functional channel densities (NT) but were accompanied by a transient decrease of Po only in tissues that were prestimulated with aldosterone. Zero time control values of Po averaged 0.52 +/- 0.05 and 0.51 +/- 0.05 in unstimulated and aldosterone-stimulated tissues, respectively, and decreased transiently in aldosterone-stimulated tissues at 7 min to 0.25 +/- 0.05, with return to 0.53 +/- 0.07 at 17 min. Thereafter, P o decreased slowly in unstimulated and stimulated tissues to 0.38 +/- 0.04 and 0.27 +/- 0.05, respectively, about two hours after treating the tissues with PGE2. From measured increases of N T of 476 +/- 47% in unstimulated tissues at 17 min and 373 +/- 69% in stimulated tissues at 7 min, NT underwent a secondary transient decrease remaining however, well above zero time control values for the duration of the 2 h experimental periods. Accordingly, PGE 2 stimulates Na+ transport in A6 epithelia both acutely and chronically by increase of the density of functional ENaCs at the apical membranes of these cells.
Use this login method if you
don't
have an
@illinois.edu
email address.
(Oops, I do have one)
IDEALS migrated to a new platform on June 23, 2022. If you created
your account prior to this date, you will have to reset your password
using the forgot-password link below.
