The purpose of this study was to characterize the transport mechanisms in endometrial epithelial cells that are responsible for regulation of Na and K concentrations in uterine luminal fluid. Porcine endometrial tissues were mounted in Ussing chambers and bathed in plasmalike Ringer solution. The mean basal short-circuit current (Isc) was 40 microA/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 analogues showed a rank order of potency of benzamil > amiloride > 5-(N-methyl-N-isobutyl)-amiloride in blocking the Isc, with no response to ethylisopropylamiloride. Na channel immunoreactivity was localized to the apical membrane of surface epithelial cells. The Na-to-K selectivity ratio of the amiloride-sensitive Na channel was calculated to be 6.4:1. Prostaglandin (PG) F2 alpha or 8-(chlorophenylthio)-adenosine 3',5'-cyclic monophosphate (CPT-cAMP) added to the luminal solution stimulated a twofold increase in Isc that 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 that 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.
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