Cellular mechanisms of adrenaline-stimulated anion secretion by the mouse endometrial epithelium

The uterine fluid composition is largely determined by the absorptive and s ecretory activities of the endometrial epithelium. The present study explor ed the cellular mechanisms involved in adrenaline-stimulated anion secretio n across the cultured mouse endometrial epithelium using the short-circuit current (I-SC) technique in conjunction with transporter inhibitors and cha nnel blockers, Cultured endometrial epithelial monolayers responded to baso lateral application of adrenaline with an increase in I-SC, which was attri butable to both Cl- and HCO3 secretion. When extracellular Cl- or HCO3 was removed, the adrenaline-induced response, as measured by the total charge t ransfer per unit area, was reduced to 53% and 46%, respectively, When both Cl- and HCO3- were absent from the bathing solutions, the adrenaline-induce d response was reduced to only 2% of the response when both ions were prese nt, indicating substantial contribution of Cl and HCO3 secretion to the adr enaline-stimulated response. Cellular mechanisms, e.g., transporters and io n channels, involved in Cl- or HCO3- secretion were investigated separately . Cl- secretion was found to depend on the activities of basolaterally loca ted Na+-K+-ATPase, Na+-K+-2Cl cotransporter, and K+ channels, while evidenc e suggested that HCO3- secretion depends substantially on basolaterally sit uated Na+-HCO3- cotransporter and Na+-H+ exchanger. Similar to what was see n for Cl- exit, a large portion of HCO3- appeared to exit apically through anion channels. The results indicate that the uterine fluid composition in the mouse may be regulated by adrenaline through stimulation of both Cl- an d HCO3- secretion and may be fine-tuned through an elaborate operation of d ifferent cellular mechanisms.