Mechanisms of electrolyte transport across the endometrium i.
regulation by pgf2[alpha] and camp.
Vetter, Alisen E., and Scott M. O'grady.
Department of Veterinary PathoBiology, 295 Animal
Science/Veterinary Medicine Building, University of Minnesota, St.
Paul, Minnesota 55108, Departments of Physiology and Animal Science,
495 Animal Science/Veterinary Medicine Building, University of
Minnesota, St. Paul, Minnesota 55108
APStracts 2:0334C, 1995.
The purpose of this study was to characterize the transport mechanisms
in endometrial epithelial cells which are responsible for regulation
of Na and K concentrations in uterine luminal fluid. Porcine
endometrial tissues were mounted in Ussing chambers and bathed in
plasma-like Ringer solution. The mean basal short-circuit current
(Isc) was 40 [mu]Amps/cm2, and the mean tissue conductance was 3.6
mS/cm2. Addition of amiloride to the luminal solution inhibited 86%
of the basal Isc. Concentration-response experiments using amiloride
analogs showed a rank order of potency of
benzamil&GTamiloride&GTMIA in blocking the Isc, with no
response to EIPA. Na channel immunoreactivity was localized to the
apical membrane of surface epithelial cells. The Na:K selectivity
ratio of the amiloride-sensitive Na channel was calculated to be
6.4:1. PGF2[alpha] or 8-cpt cAMP added to the luminal solution
stimulated a two-fold increase in Isc which was inhibited by
pretreatment with amiloride. Experiments using both amphotericin B
-permeabilized tissues and intact tissues showed that PGF2[alpha] and
cAMP increased Na absorption by activation of basolateral K channels.
Treatment of the luminal solution with 4-aminopyridine produced an
effect on Isc which was consistent with block of K secretion and a
subsequent decrease in Na absorption. These experiments showed that
Na and K transport are tightly coupled processes occurring under
basal conditions in surface endometrial epithelial cells and that
these processes are regulated by PGF2[alpha] and cAMP.
Received 10 April 1995; accepted in final form 25 August 1995.
APS Manuscript Number C199-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 September 1995.