Parasympathetic reflex vasodilatation in the masseter muscle compensates for carotid hypoperfusion during the vagus-mediated depressor response.

Parasympathetic vasodilatation in the orofacial area is thought to be an important factor in the regulation of blood flow in the common carotid artery (CABF), and disturbances in parasympathetic vasodilatations may be related to impairment of the CABF inducing craniofacial ischemia. We hypothesized that the parasympathetic vasodilatation in the masseter muscle evoked by a vagus-mediated reflex is involved in the maintenance of the CABF during the vagus-mediated depressor response. In the present study, we compared changes in blood flow in the masseter muscle (MBF) and CABF, and systemic arterial blood pressure (SABP) evoked by electrical stimulation of the central cut end of the cervical vagus nerve (cVN) in anesthetized and sympathectomized rats. Electrical stimulation of the cVN in the sympathectomized animals caused an increase in MBF followed by a CABF increase, although it simultaneously induced a decrease in SABP. These increases in blood flow changed to decreases after intravenous administration of atropine (100 μg/kg), while pretreatment with atropine had no effect on the changes in SABP. Microinjection (50 nl/site) of the muscimol (1mM), into the nucleus of the solitary tract, which is involved in reflex cardiovascular regulation, markedly inhibited the cVN stimulation-induced MBF increase. Our results indicate that vagal-parasympathetic vasodilatation in the masseter muscle compensates for carotid hypoperfusion during the vagus-mediated depressor response, and that GABAergic neurons may be involved in the inhibition of this response. This inhibition may result in the impairment of CABF, suggesting an important role in the etiology of neurally mediated syncope.