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Involvement of Na⁺-HCO₃^- Cotransporter in Mediating Cyclic Adenosine 3',5'-Monophosphate-Dependent HCO₃^- Secretion by Mouse Endometrial Epithelium¹

^a Epithelial Cell Biology Research Center ^b Department of Physiology, Faculty of Medicine, Chinese University of Hong Kong, Shatin, Hong Kong ^c Shanghai Institute of Planned Parenthood Research, Shanghai, China

The present study investigated the involvement of Na⁺-HCO₃^- cotransporter in mediating cAMP-stimulated HCO₃^- secretion across the cultured mouse endometrial epithelium using the short-circuit current (I_SC) technique and intracellular pH measurement. Forskolin stimulated a rise in the I_SC, 55.6% and 52.1% of which could be reduced by the removal of extracellular Cl^- or by eliminating the contribution of Cl^- secretion by bumetanide, an inhibitor of Na⁺-K⁺-2Cl^- cotransporter, respectively. More than 80% reduction in the forskolin-induced I_SC was obtained when both Cl^- and HCO₃^- in the bath were removed or in HCO₃^--free solution with bumetanide, indicating that the I_SC depended on both Cl^- and HCO₃^-. The presence of the Na⁺ channel-blocker amiloride in the apical solution did not reduce the forskolin-induced I_SC; however, the I_SC could be abolished by removing Na⁺ from the bathing solution, suggesting that the Cl^-- and HCO₃^--dependent I_SC was also dependent on basolateral Na⁺. The forskolin-stimulated I_SC could be reduced 43.6% by removal of HCO₃^- and 47.9% by a Na⁺-HCO₃^--cotransporter inhibitor, dihydrogen-4,4'-didsothiocyanostilbene-2,2'-disulfonic acid (H₂DIDS). The inhibitory effect of H₂DIDS was observed in Cl^--free solution, but not when HCO₃^- was removed, thus confirming its effect on HCO₃^--dependent transport. Intracellular pH measurements demonstrated that the recovery from cellular acidification depended on the presence of both basolateral Na⁺ and HCO₃^-, further indicating the involvement of Na⁺-HCO₃^- cotransporter. Reverse transcription-polymerase chain reaction experiments confirmed the expression of Na⁺-HCO₃^- cotransporter in the mouse endometrium. The results suggest that basolaterally located Na⁺-HCO₃^- cotransporter is involved in mediating cAMP-stimulated HCO₃^- secretion across the mouse endometrial epithelium.

First decision: 19 October 2001.

¹ The work was carried out at the Epithelial Cell Biology Research Center and was supported by the direct grant (2040775) and strategic research program of The Chinese University of Hong Kong and National 973 Research Project of China.

² Correspondence. FAX: 852 2603 5022; hsiaocchan{at}cuhk.edu.hk