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Norepinephrine transporter blocker atomoxetine increases salivary alpha amylase

It has been suggested that central norepinephrine (NE) activity may be inferred from increases in salivary alpha-amylase (SAA), but data in favor of this proposition are limited. We administered 40mg of atomoxetine, a selective NE transporter blocker that increases central NE levels, to 24 healthy a...

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Hauptverfasser: Warren, Christopher M. (VerfasserIn) , Brink, Ruud L. van den (VerfasserIn) , Bosch, Jos A. (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 31 January 2017
In: Psychoneuroendocrinology
Year: 2017, Jahrgang: 78, Pages: 233-236
ISSN:1873-3360
DOI:10.1016/j.psyneuen.2017.01.029
Online-Zugang:Verlag, Volltext: http://dx.doi.org/10.1016/j.psyneuen.2017.01.029
Verlag, Volltext: http://www.sciencedirect.com/science/article/pii/S0306453016305832
Volltext
Verfasserangaben:Christopher M. Warren, Ruud L. van den Brink, Sander Nieuwenhuis, Jos A. Bosch

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520 |a It has been suggested that central norepinephrine (NE) activity may be inferred from increases in salivary alpha-amylase (SAA), but data in favor of this proposition are limited. We administered 40mg of atomoxetine, a selective NE transporter blocker that increases central NE levels, to 24 healthy adult participants in a double-blind, placebo-controlled cross-over design. Atomoxetine administration significantly increased SAA secretion and concentrations at 75-180min after treatment (more than doubling baseline levels). Consistent with evidence that elevation in central NE is a co-determinant of hypothalamic-pituitary-adrenal axis activity, salivary cortisol also approximately doubled at the same time points. Moreover, changes in salivary cortisol positively correlated with SAA (0.44<rho<0.56), bolstering the position that the origin of the changes in SAA reflect central NE. This work points toward the potential value of SAA as an inexpensive and non-invasive procedure to obtain information about activation of the central NE system. 
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