SGLT1 protein expression in plasma membrane of acinar cells correlates with thesympathetic outflow to salivary glands in diabetic and hypertensive rats.

摘要

Salivary gland dysfunction is a feature in diabetes and hypertension. Wehypothesized that sodium-glucose cotransporter 1 (SGLT1) participates in salivarydysfunctions through a sympathetic- and protein kinase A (PKA)-mediated pathway. In Wistar-Kyoto (WKY), diabetic WKY (WKY-D), spontaneously hypertensive (SHR),and diabetic SHR (SHR-D) rats, PKA/SGLT1 proteins were analyzed in parotid andsubmandibular glands, and the sympathetic nerve activity (SNA) to the glands was monitored. Basal SNA was threefold higher in SHR (P < 0.001 vs. WKY), anddiabetes decreased this activity (50%, P < 0.05) in both WKY and SHR. Thecatalytic subunit of PKA and the plasma membrane SGLT1 content in acinar cellswere regulated in parallel to the SNA. Electrical stimulation of the sympathetic branch to salivary glands increased (30%, P < 0.05) PKA and SGLT1 expression.Immunohistochemical analysis confirmed the observed regulations of SGLT1,revealing its location in basolateral membrane of acinar cells. Taken together,our results show highly coordinated regulation of sympathetic activity upon PKAactivity and plasma membrane SGLT1 content in salivary glands. Furthermore, thepresent findings show that diabetic- and/or hypertensive-induced changes in thesympathetic activity correlate with changes in SGLT1 expression in basolateralmembrane of acinar cells, which can participate in the salivary glandsdysfunctions reported by patients with these pathologies.