SLC5A1 in rat parotid and submandibular with hypertension and diabetes

Objectives: There is little information concerning salivary gland function in hypertensive persons before anti-hypertensive therapy; however, some studies have demonstrated decrease in whole non-stimulated salivary secretion. We have previously observed alteration in SLC5A1 gene expression and subcellular localization of SGLT1 protein in parotid and submandibular glands of diabetic Wistar rats. This may be related to impaired glandular function of diabetic subjects, since the SGLT1 is also responsible for water transport. We propose that hypertension associated with diabetes, with high sympathetic tonus, might interfere in the SLC5A1 gene expression, thus exacerbating functional damage of the salivary glands. The purpose of the present study was to investigate the SLC5A1 gene expression in parotid and submandibular of spontaneously hypertensive rats (SHR) with or without diabetes. Methods: Wistar Kyoto (K), SHR and SHR with diabetes (SHR+DM) were investigated. Diabetes was induced by i.v. injection of aloxan (38 mg/kg-body weight) 30 days before the study. On the day of sacrifice, parotid and submandibular glands were harvested for SGLT1 mRNA (RT-PCR) and protein (Western blotting) analysis. Results: The analysis of results (One-way ANOVA-Newman-Keuls) showed that, compared to K rats, in SHR the SGLT1 mRNA and protein expression increased only in parotid (by 49.7% and 210.6%, P<0.05 and P<0.001 vs. K, respectively). When diabetes was induced in SHR, the amount of SGLT1 mRNA and protein increased by 24.1% and 24.8%, respectively, in parotid (P>0.05) and by 45.7% and 110.2% in submandibular (P<0.05 and P<0.01 vs SHR, respectively). Conclusion: The results indicate that the sympathetic hyperactivity and or hypertension of SHR induce the increase in SLC5A1 gene expression in parotid, which was not altered by the association of diabetes. On the other hand, in submandibular, the SLC5A1 gene expression is unaltered in SHR, however, when diabetes is associated, increased expression is observed.

Financial Support: FAPESP 06/60833-2, 07/54805-9, 06/60101-1.