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Defective cellular trafficking of aquaporin-5 (AQP5) to the apical plasma membrane (APM) in salivary glands is associated with the loss of salivary fluid secretion. To examine mechanisms of α1-adrenoceptor (AR)-induced trafficking of AQP5, immunoconfocal microscopy and Western blot analysis were used to analyze AQP5 localization in parotid tissues stimulated with phenylephrine under different osmolality. Phenylephrine-induced trafficking of AQP5 to the APM and lateral plasma membrane (LPM) was mediated via the α1A-AR subtype, but not the α1B- and α1D-AR subtypes. Phenylephrine-induced trafficking of AQP5 was inhibited by ODQ and KT5823, inhibitors of nitric oxide (NO)-stimulated guanylcyclase (GC) and protein kinase (PK) G, respectively, indicating the involvement of the NO/ soluble (c) GC/PKG signaling pathway. Under isotonic conditions, phenylephrine-induced trafficking was inhibited by La3+, implying the participation of store-operated Ca2+ channel. Under hypotonic conditions, phenylephrine-induced trafficking of AQP5 to the APM was higher than that under isotonic conditions. Under non-stimulated conditions, hypotonicity-induced trafficking of AQP5 to the APM was inhibited by ruthenium red and La3+, suggesting the involvement of extracellular Ca2+ entry. Thus, α1A-AR activation induced the trafficking of AQP5 to the APM and LPM via the Ca2+/ cyclic guanosine monophosphate (cGMP)/PKG signaling pathway, which is associated with store-operated Ca2+ entry.

Salivary glands in elderly individuals commonly exhibit morphological changes and dysfunction resulting in xerostomia. Long-term (4-week) drinking of whey prevented and/or restored age-dependent decline of salivary volume and protein concentration, and atrophy of sublingual glands (SLGs) significantly in 88-week-old rats. The transcripts of 42 genes were up-regulated and 7 genes were down-regulated by more than 1.5-fold change with FDR ≦ 0.1 after whey-drinking. The expression levels of genes associated with salivary proteins and tissue repair were significantly increased, while those associated with lipid metabolism were decreased. Venn diagram analysis revealed that expressions of 13 genes, including Tcfap2b and Abpa, were induced significantly by whey-drinking. Furthermore, secretory protein levels in SLGs and saliva were revealed by immunoblot analysis. This is the first study to report that whey-administration can prevent and/or restore age-dependent atrophy and functional decline of SLGs in relation to gene expression and thus may serve as a functional food ingredient.

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