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Am J Physiol Gastrointest Liver Physiol 286: G312-G320, 2004. First published September 4, 2003; doi:10.1152/ajpgi.00158.2003
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MUCOSAL BIOLOGY

Cl-/HCO3- exchange is acetazolamide sensitive and activated by a muscarinic receptor-induced [Ca2+]i increase in salivary acinar cells

Ha-Van Nguyen,1 Alan Stuart-Tilley,2 Seth L. Alper,3 and James E. Melvin1

1Center for Oral Biology, Aab Institute of Biomedical Sciences, University of Rochester Medical Center, Rochester, New York 14642;2Molecular Medicine and Renal Units, Beth Israel Deaconess Medical Center, and3Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215

Submitted 4 April 2003 ; accepted in final form 30 August 2003

Large volumes of saliva are generated by transepithelial Cl- movement during parasympathetic muscarinic receptor stimulation. To gain further insight into a major Cl- uptake mechanism involved in this process, we have characterized the anion exchanger (AE) activity in mouse serous parotid and mucous sublingual salivary gland acinar cells. The AE activity in acinar cells was Na+ independent, electroneutral, and sensitive to the anion exchange inhibitor DIDS, properties consistent with the AE members of the SLC4A gene family. Localization studies using a specific antibody to the ubiquitously expressed AE2 isoform labeled acini in both parotid and sublingual glands. Western blot analysis detected an ~170-kDa protein that was more highly expressed in the plasma membranes of sublingual than in parotid glands. Correspondingly, the DIDS-sensitive exchanger activity was significantly greater in sublingual acinar cells. The carbonic anhydrase antagonist acetazolamide markedly inhibited, whereas muscarinic receptor stimulation enhanced, the exchanger activity in acinar cells from both glands. Intracellular Ca2+ chelation prevented muscarinic receptor-induced upregulation of the AE, whereas raising the intracellular Ca2+ concentration with the Ca2+-ATPase inhibitor thapsigargin mimicked the effects of muscarinic receptor stimulation. In summary, carbonic anhydrase activity was essential for regulating exchange in salivary gland acinar cells. Moreover, muscarinic receptor stimulation enhanced AE activity through a Ca2+-dependent mechanism. Such forms of regulation may play important roles in modulating fluid and electrolyte secretion by salivary gland acinar cells.

secretion; carbonic anhydrase; exchanger; calcium regulation


Address for reprint requests and other correspondence: J. E. Melvin, Center for Oral Biology, Univ. of Rochester, Medical Center Box 611, 601 Elmwood Ave., Rochester, New York 14642 (E-mail: james_melvin{at}urmc.rochester.edu).




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