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Journal of Dental Research, Vol. 85, No. 9, 839-843 (2006)
DOI: 10.1177/154405910608500912

Biological

Desipramine Inhibits Na+/H+ Exchanger in Human Submandibular Cells

S.-Y. Choi1,4, J. Li1,4, S.-H. Jo2, S.J. Lee1, S.B. Oh1, J.-S. Kim1, J.-H. Lee3 and K. Park1,*

1 Department of Physiology and
3 Department of Oral and Maxillofacial Surgery, School of Dentistry and Dental Research Institute, Seoul National University, Seoul 110-749, Korea; and
2 Department of Physiology, Cheju National University College of Medicine, Jeju 690-756, Korea

Correspondence: * corresponding author, kppark{at}snu.ac.kr

A common and significant side-effect of the antidepressant desipramine is xerostomia (dry mouth). We investigated the effect of desipramine on Na+/H+ exchanger, which is an important modulator of salivary secretion. In dissociated human submandibular acinar cells, desipramine inhibited intracellular pH recovery in a concentration-dependent manner. Likewise, 5-(N-ethyl-N-isopropyl)amiloride (EIPA), a Na+/H+ exchanger inhibitor, had the same effect as desipramine, whereas the effect of 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS), a Na+/HCO3– co-transporter inhibitor, was not dramatic. Although desipramine is known to inhibit catecholamine re-uptake, desipramine also inhibited pH recovery in the human submandibular gland cell line, HSG cells, which lack nerve inputs. Our results suggest that desipramine directly inhibits Na+/H+ exchange in human submandibular glands without the involvement of catecholamine re-uptake, revealing the cellular mechanism of desipramine-evoked xerostomia.

Key Words: desipramine • xerostomia • intracellular pH • Na+/H+ exchange • secretion


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