Age-related decrease of cholinergic parasympathetic reflex vasodilation in the rat masseter muscle.

Skeletal muscle hemodynamics, including that in jaw muscles, is an important in their functions and is modulated by aging. Marked blood flow increases mediated by parasympathetic vasodilation may be important for blood flow in the masseter muscle (MBF); however, the relationship between parasympathetic vasodilation and aging is unclear. We examined the effect of aging on parasympathetic vasodilation evoked by trigeminal afferent inputs and their mechanisms by investigating the MBF during stimulation of the lingual nerve (LN) in young and old urethane-anesthetized and vago-sympathectomized rats. Electrical stimulation of the central cut end of the LN elicited intensity- and frequency-dependent increases in MBF in young rats, while these increases were significantly reduced in old rats. Increases in the MBF evoked by LN stimulation in the young rats were greatly reduced by hexamethonium and atropine administration. Increases in MBF in young rats were produced by exogenous acetylcholine in a dose-dependent manner, whereas acetylcholine did not influence the MBF in old rats. Significant levels of muscarinic acetylcholine receptor type 1 (MR1) and type 3 (MR3) mRNA were observed in the masseter muscle in young rats, but not in old rats. Our results indicate that cholinergic parasympathetic reflex vasodilation evoked by trigeminal afferent inputs to the masseter muscle is reduced by aging and that this reduction may be mediated by suppression of the expression of MR1 and MR3 in the masseter muscle with age.

Effect of the parasympathetic vasodilation on temperature regulation via trigeminal afferents in the orofacial area.

The skin temperature (Tm) of the orofacial area influences orofacial functions and is related to the blood flow (BF). Marked increases in BF mediated by parasympathetic vasodilation may be important for orofacial Tm regulation. Therefore, we examined the relationship between parasympathetic reflex vasodilation and orofacial Tm in anesthetized rats. Electrical stimulation of the central cut end of the lingual nerve (LN) elicited significant increases in BF and Tm in the lower lip. These increases were significantly reduced by hexamethonium, but not atropine. VIP agonist increased both BF and Tm in the lower lip. The activation of the superior cervical sympathetic trunk (CST) decreased BF and Tm in the lower lip; however, these decreases were significantly inhibited by LN stimulation. Our results suggest that parasympathetic vasodilation plays an important role in the maintaining the hemodynamics and Tm in the orofacial area, and that VIP may be involved in this response.

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

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.