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1 Department of Medicine, School of Medicine, University of California Los Angeles, Los Angeles, CA, USA; CURE: Digestive Research Center, Los Angeles, CA, USA
2 San Fernando Valley Internal Residency Program, Los Angeles, CA, USA
3 Greater Los Angeles Veterans Affairs Healthcare System, University of California Los Angeles, Los Angeles, CA, USA
4 Department of Biomathematics, University of California Los Angeles, Los Angeles, CA, USA
5 Greater Los Angeles Veterans Affairs Healthcare System, University of California Los Angeles, Los Angeles, CA, USA; Department of Medicine, School of Medicine, University of California Los Angeles, Los Angeles, CA, USA; CURE: Digestive Research Center, Los Angeles, CA, USA
* To whom correspondence should be addressed. E-mail: jake{at}ucla.edu.
We examined the effect of inhibition of sodium-proton exchange (NHE) on duodenal bicarbonate secretion (DBS) in rats in order to further understand DBS regulation. DBS was measured using the pH-stat method and by using CO2 sensitive electrodes. 50 µM dimethyl amiloride, a concentration that selectively inhibits the NHE isoforms NHE1 and NHE2, but not NHE3, did not affect DBS. Nevertheless, 3 mM dimethyl amiloride, a higher concentration that inhibits NHE1, NHE2 and NHE3, significantly increased DBS. Moreover, S1611 and S3226, both specific inhibitors of NHE3 only, or perfusion with sodium-free solutions, dose-dependently increased DBS, as measured by pH-stat and CO2 sensitive electrode, without affecting intracellular pH. Co-perfusion with 0.1 µM indomethacin, 0.5 mM DIDS or 1 mM methazolamide did not affect S3226-induced DBS. Nevertheless, co-perfusion with 0.1 and 0.3 mM 5-nitro-2-(3-phenylpropylamino) benzoic acid, which inhibits CFTR, dose-dependently inhibited S3226-induced DBS. In conclusion, only specific apical NHE3 inhibition increased DBS, whereas prostaglandin synthesis, Na+: HCO3- cotransporter activation, or intracellular HCO3- formation by carbonic anhydrase were not involved. Since NHE3 inhibition increased DBS was inhibited by an anion channel inhibitor, and since reciprocal -CFTR regulation has been previously shown between NHE3 and apical membrane anion transporters, speculate that NHE3 inhibition increased DBS by altering anion transporter function.
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