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Abstract
Tricyclic antidepressants (TCA) are well-known xerogenic drugs, while antidepressants
such as selective serotonin reuptake inhibitors (SSRI) are considered less xerogenic.
The antimuscarinic effect of the TCAs has been considered to be the principal mechanism
causing a dry mouth. Although the muscarinic receptor is commonly targeted by xerogenic
pharmaceuticals, the salivation reflex arc may be affected at other levels as well.
We currently wondered whether or not antidepressants exert an inhibition of the salivary
reflex not only at the glandular level but at a central level as well. In this study,
the effects of a TCA (clomipramine), a SSRI (citalopram) and a serotonin-noradrenaline
reuptake inhibitor (SNRI; venlafaxine) were examined on reflex- (0.5M citric acid
applied on the tongue) and methacholine-evoked salivary secretion. While all three
compounds inhibited citric acid-evoked secretion (-40 to -60% at 5mg/kg i.v. of the
antidepressants), only clomipramine inhibited methacholine-evoked secretion (-30%
at 5mg/kg i.v.). On the contrary, both citalopram and venlafaxine increased the methacholine-evoked
secretion (+44 to 49%). This was particularly obvious for the salivary protein output
(>200%). In the presence of α- and β-adrenoceptor antagonists, the citalopram- and
venlafaxine-induced increases were reduced. Thus, antidepressants irrespective of
type may exert xerogenic effects by inhibiting the salivary reflex in the central
nervous system. However, while TCAs may also hamper the secretory response by antimuscarinic
effects, the SSRI and the SNRI groups of pharmaceuticals seem to lack this additional
xerogenic mechanism indicating a better therapeutic profile and better opportunities
for pharmacological treatment of drug-induced xerostomia.