Abstract
Luminal acid is the most potent physiologic stimulus for duodenal bicarbonate secretion (DBS) ([1). Indomethacin inhibits acid-induced DBS, consistent with the involvement of cyclooxygenase (COX) ([2). Also, protein kinase A (PKA) is thought to be involved, since cAMP stimulates the cystic fibrosis transmembrane conductance regulator (CFTR), a candidate apical HC03 - channel and the basolateral sodium bicarbonate cotransporter (NBC) ([3, [4). DBS also cAMP dependent. Nevertheless, little is known about the involvement of other kinases, such as protein kinase C (PKC) and tyrosine kinase (TK), in acid-induced DBS. We thus tested the hypothesis that acid-induced DBS requires intracellular signaling pathways by testing the effects of protein kinase inhibitors, staurosporine for PKC, H-89 for PKA and genistein for TK on acid-induced DBS in rats.
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Furukawa, O., Hirokawa, M., Guth, P.H., Engel, E., Kaunitz, J.D. (2002). Role of Protein Kinases on Acid-Induced Duodenal Bicarbonate Secretion in Rats. In: Urushidani, T., Forte, J.G., Sachs, G. (eds) Mechanisms and Consequences of Proton Transport. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0971-4_17
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DOI: https://doi.org/10.1007/978-1-4615-0971-4_17
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