Interactions between β-adrenergic vasodilation and cervical sympathetic nerves are mediated by α2-adrenoceptors in the rat masseter muscle

Abstract

Neural and humoral autonomic mechanisms may be important in the maintenance of blood flow in the masseter muscle (MBF). However, their interactions remain unclear. In this study, we examined interactions between neural and humoral regulation of MBF and investigated the mechanisms mediating these interactions in urethane-anesthetized rats. Stimulation of the adrenal nerve (AN) projecting to the adrenal medulla increased MBF, and this increase was mediated by β-adrenoceptors. Sectioning of the superior cervical sympathetic trunk (CST) significantly inhibited increases in MBF induced by AN stimulation during high activity in the CST, but not during low activity. AN stimulation with clonidine after CST sectioning induced a significant increased in MBF, however phenylephrine had no observable effect. Pretreatment with yohimbine or propranolol significantly inhibited the increase in the MBF. Our results suggest an interaction between β-adrenergic vasodilation evoked by circulating adrenaline and the cervical sympathetic nerves that is mediated by α2-adrenoceptors in the masseter muscle.

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

“…The anesthetized animals were intubated, paralyzed by intravenous (iv) injection of pancuronium bromide (Mioblock; Organon, Teknika, the Netherlands; 0.6 mg/kg initially, supplemented with 0.4 mg/kg every hour or so after testing the level of anesthesia; see below), and artificially ventilated via a tracheal cannula with a mixture of 50% air and 50% O 2 . The ventilator (model SN-480-7; Shinano, Tokyo, Japan) was set to deliver a tidal volume of 8.5-10 cm 3 /kg at a rate of 20-23 breaths/min, and the end-tidal concentration of CO 2 was determined by means of an infrared analyzer (Capnomac Ultima; Datex, Helsinki, Finland), as reported elsewhere [15,17,22]. This method of continuous ventilation has been shown to maintain the end-tidal concentration of CO 2 at 40-45 mmHg.…”

“…Previously, the activation of parasympathetic vasodilator fibers has been reported to occur through trigeminal afferent inputs leading to a rapid and marked increase in BF in orofacial tissues, such as lower lip [16], jaw muscles [17,18] and salivary glands [15,19]. On the other hand, sympathetic vasoconstriction is under tonic control from the superior cervical sympathetic trunk (CST) [20][21][22]. Therefore, parasympathetic vasodilation mediated through the trigeminal reflex mechanisms and interaction between parasympathetic and sympathetic fibers may play an important role in the regulation of both hemodynamics and T m in the orofacial area.…”

The correlation between SNPs within the gene of adrenergic receptor and neuropeptide Y and risk of cervical vertigo

“…The adjustment of vessel caliber was indicated as a major regulatory factor engendering PCI, and the vasoconstrictive effects of sympathetic nerves were realized through the neurotransmitters released from postganglionic fibers, including noradrenaline (NA) and neuropeptide Y (NPY) . Taking NA for example, when sympathetic nerves were activated, the combining capacity of NA and α adrenergic receptor [eg, adrenoceptor alpha 1A (ADRA1A)] within smooth muscles around vessel walls outperformed that of NA and β adrenergic receptor [eg, adrenoceptor beta 2 (ADRB2) and adrenoceptor beta 1 (ADRB1)], rendering the occurrence of vasomotor reaction.…”