Relationship between impaired parasympathetic vasodilation and hyposalivation in parotid glands associated with type 2 diabetes mellitus.

Abstract

We examined the relationship between hemodynamics in the three major salivary glands and salivary secretion in urethane-anesthetized and sympathectomized type 2 diabetic and nondiabetic rats via laser speckle imaging and by collecting the saliva. Lingual nerve stimulation elicited rapid increases in glandular blood flow and induced salivary secretion from the three glands in both diabetic and nondiabetic rats. In the parotid gland, the magnitude of blood flow increase and salivary secretion was significantly lower in the diabetic rats when compared with the nondiabetic rats; however, this was not observed in the other glands. Although the intravenous administration of acetylcholine increased blood flow in the parotid gland in a dose-dependent manner, the response was significantly lower in the diabetic rats when compared with the nondiabetic rats. Similarly, mRNA expression levels of M1 and M3 muscarinic acetylcholine receptors in the parotid gland were relatively lower in the diabetic rats compared with the nondiabetic rats. Our results indicate that type 2 diabetes impairs parasympathetic vasodilation and salivary secretion in the parotid gland and suggest that disturbances in the cholinergic vasodilator pathway may contribute to the underlying mechanisms involved in the disruption of parasympathetic nerve-mediated glandular vasodilation.