Response to: “Is an increase in duodenal bicarbonate concentration after STa really enhanced bicarbonate ion secretion?” Zachary M. Sellers and Hui Dong 1 Division of Gastroenterology, Department of Medicine, School of Medicine, University of California, San Diego, La Jolla, California, USA 1 Correspondence: h2dong@ucsd.edu Thank you for the opportunity to respond to comments raised by one of your readers regarding our manuscript, “Heat-stable enterotoxin of Escherichia coli (STa) can stimulate duodenal HCO 3 − secretion via a novel GC-C- and CFTR-independent pathway (1) ⇓ ” . With two currently published manuscripts on this topic, we have performed many experiments using multiple well validated in vitro and in vivo methods (including pH stat, back-titration and CO 2 -sensitive electrode methods) to measure STa-stimulated duodenal HCO 3 − secretion in the absence of CFTR function (1 ⇓ , 2) ⇓ . However, the reader’s concern about the involvement of Na + /H + exchange (NHE) is valid. Studies have shown that inhibition of NHE produces an increase in measurable duodenal HCO 3 − (3 ⇓ , 4) ⇓ , which can be at least partially attenuated by inhibition of CFTR (4) ⇓ . Thus, when measuring HCO 3 − one
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Response to: “Is an increase in duodenal bicarbonate concentration after STa really enhanced bicarbonate ion secretion?”
Sellers, Zachary M.; Dong, Hui
Follow The FASEB Journal
, Volume 23 (2): 295
Fed of American Socs for Experimental Biology – Feb 1, 2009
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