Takeharu Niioka

Evidence for parasympathetic vasodilator fibres in the rat masseter muscle

The present study was designed to examine (1) whether there are vasodilator fibres in the masseter muscle, and (2) if there are, to establish the neural pathways mediating these responses in urethane‐anaesthetized rats. Electrical stimulation of the central cut end of the lingual nerve (LN) elicited intensity‐ and frequency‐dependent increases of the blood flow in the masseter muscle (MBF) and lower lip (LBF). Increases in both the MBF and LBF evoked by the LN stimulation were reduced by hexamethonium in a dose‐dependent manner (1–10 mg kg−1). Pretreatment with phentolamine or propranolol at a dose of 100 μg kg−1 had no effect on the increases in either MBF or LBF evoked by LN stimulation. Pretreatment with atropine (100 μg kg−1) significantly reduced the MBF increase induced by LN stimulation, but not that in the LBF. The sectioning of the superior cervical sympathetic trunk did not affect the responses. MBF increases occurred with electrical stimulation of the trigeminal ganglion, and these increases were significantly reduced by the administration of hexamethonium and atropine. Lidocaine microinjection into the trigeminal spinal nucleus or salivatory nuclei caused a significant attenuation of the LN‐induced MBF increases. When wheat germ agglutinin–horseradish peroxidase (WGA–HRP) was injected into the masseter muscle, labelled neurones were abundantly observed in the otic ganglion. The present study indicates that there are parasympathetic cholinergic and noncholinergic vasodilator fibres originating from cell bodies in the otic ganglion in the rat masseter muscle. The MBF increase evoked by activation of the parasympathetic fibres occurred via the trigeminal mediated reflex, suggesting that the novel parasympathetic vasodilator response may play an important role in the regulation of the haemodynamics of jaw muscles.

Vagal visceral inputs to the nucleus of the solitary tract: Involvement in a parasympathetic reflex vasodilator pathway in the rat masseter muscle

The present study examined whether vagal visceral inputs are involved in parasympathetic reflex vasodilatation in the masseter muscle in urethane-anesthetized and cervically sympathectomized rats. Electrical stimulation of the central cut end of the cervical vagus nerve (VN) including visceral afferent fibers, which consisted of cervical/thoracic branches (heart and lungs) and abdominal branches (entire gastrointestinal tract), elicited intensity- and frequency-dependent increases of blood flow in the masseter muscle (MBF). Activation of the abdominal VN inferior to the diaphragm failed to affect the MBF. MBF increases evoked by cervical VN stimulation were reduced significantly by hexamethonium. Pretreatment with atropine reduced the MBF increase evoked by VN stimulation significantly, whereas pretreatment with either propranolol or phentolamine had no effect on the response. MBF increases occurred with electrical stimulation of nucleus of the solitary tract (NTS), and these increases were significantly reduced by the administration of hexamethonium and atropine. MBF increases also occurred after microinjection of glutamate into the NTS in a dose-dependent manner. Microinjection of muscimol into the NTS caused a significant attenuation of the VN stimulation-induced MBF increases. Our results suggest that vagal visceral inputs passing to the NTS are involved in the parasympathetic reflex vasodilatation in the rat masseter muscle. The MBF increase evoked by the vagal-parasympathetic reflex mechanism occurred via visceral afferents running in the cervical VN, but not in the abdominal VN, suggesting that the vagal visceral afferents derived from cardiovascular and/or respiratory systems may play an important role in the regulation of the MBF.

Difference between male and female rats in cholinergic activity of parasympathetic vasodilatation in the masseter muscle

We compared the changes in blood flow of the masseter muscle (MBF), lower lip (LBF) and common carotid artery (CCABF) evoked by electrical stimulation of the lingual nerve (LN) in order to examine whether high cholinergic activity of parasympathetic vasodilatation in females is specific for the masseter muscle, and whether sex-associated differences in cholinergic parasympathetic vasodilatation affect the regulation of blood flow to the orofacial area from the CCABF in urethane-anaesthetized, vago-sympathectomized male and female rats. Increases in the MBF, LBF and CCABF evoked by LN stimulation appear to be mediated via an activation of parasympathetic reflex vasodilatation since these increases were profoundly reduced by pretreatment with the autonomic cholinergic ganglion blocker hexamethonium (10 mg/kg). Although alpha- and beta-adrenoceptor antagonists (phentolamine and propranolol, 100 microg/kg) had no effect on the LN stimulation-induced blood flow increases in either sex, a marked difference was found between males and females in the effects of the antimuscarinic agent atropine (1-100 microg/kg) on these blood flow increases. Pretreatment with atropine slightly attenuated the increase in the MBF in males, but in females it markedly reduced the increases in all three sites measured, especially in the MBF. Our results suggest that (1) cholinergic activity of the parasympathetic vasodilatation in females is higher than that in males in most orofacial tissues, but particularly in the masseter muscle and (2) cholinergic parasympathetic vasodilatations are more involved in the regulation of blood flow to the orofacial area from the CCABF in females than in males.

Circulating adrenaline released by sympathoadrenal activation elicits acute vasodilatation in the rat masseter muscle

The present study was designed to examine the effects of circulating catecholamines released by sympathoadrenal system on the haemodynamics of the masseter muscle in deeply urethane-anaesthetized, artificially ventilated, cervically vagotomized and sympathectomized rats. Intravenous administration of adrenaline induced a biphasic change of blood flow in the masseter muscle (MBF). The change of blood flow showed an initial marked increase and successive slight decrease in a dose-dependent manner (0.01-1 microg/kg). The administration of noradrenaline had no significant effect on the MBF. The increase in the MBF evoked by exogenously applied adrenaline was markedly reduced by the intravenous administration of propranolol (100 microg/kg), whereas pretreatment with either hexamethonium (10 mg/kg), atropine (100 microg/kg), or phentolamine (1 mg/kg) failed to affect the MBF increase. Electrical stimulation of splanchnic nerve (SPLN) preganglionic neurones projecting to the adrenal medulla elicited frequency-dependent (1-20 Hz) increases in the MBF. The intravenous administration of the beta(2)-adrenergic receptor selective antagonist, ICI 118551 (0.5 mg/kg), almost abolished the MBF increase induced by SPLN stimulation, but pretreatment with the beta(1)-adrenergic receptor selective antagonist, atenolol (1 mg/kg), had no effect on this response. The results of the present study indicate that circulating adrenaline elicits acute vasodilatation through a beta-adrenergic mechanism in the rat masseter muscle. Vascular beta(2)-adrenergic receptors in the masseter muscle may be activated preferentially by adrenaline released from the adrenal medulla, suggesting that the sympathoadrenal system is involved in the marked MBF increase during sympathoexcitation.

Regional differences in blood flow variation in rat masseter muscle.

Regions of a belly in a masseter muscle have been suggested to be activated independently in order to enable complex jaw-movements. However a regional difference of the masseter blood flow (MBF) is still unclear although the blood flow is one of the most important factors during activation of the muscle. The present study examined regional differences in blood flow in rat masseter muscle by comparing blood flow values at the inferior, centre, superior, anterior, and posterior regions of the muscle belly using a laser speckle imaging flowmeter with or without sympathetic and parasympathetic stimulation. Regional differences in blood flow levels were observed in each region of the masseter muscle belly during rest. Additionally, amplitudes of blood flow changes evoked by electrical stimulation of parasympathetic and sympathetic nerves differed among regions. These results demonstrate the regional differences in hemodynamics during rest, sympathetic vasoconstriction (including the recovery phase), and parasympathetic vasodilatation in rat masseter muscle.

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.

Parasympathetic vasodilator fibers in rat digastric muscle

The present study examined whether parasympathetic vasodilator fibers exist in rat jaw-opening muscles such as the digastric muscle. The mental nerve was stimulated to activate the parasympathetic vasodilator nerve in the digastric muscle. Electrical stimulation of the mental nerve elicited intensity- and frequency-dependent increases of blood flow in this muscle. These increases were markedly reduced by hexamethonium in dose- and time-dependent manners, but pretreatment with phentolamine or propranolol had no effect. Pretreatment with atropine also attenuated the increase in blood flow in digastric muscle. When retrograde fluorogold was injected into the digastric muscle, labeled neurons were observed in the otic ganglion only on the ipsilateral side, but not in the pterygopalatine ganglion of either side. These results indicate that parasympathetic vasodilator fibers originate from cell bodies in the otic ganglion in rat digastric muscle.

Involvement of vasoactive intestinal polypeptide in the parasympathetic vasodilatation of the rat masseter muscle

The parasympathetic vasodilatory fibres are known to innervate vessels in a rat masseter muscle via both cholinergic and non-cholinergic mechanisms. However, the non-cholinergic mechanisms are still unclear. Recently, vasoactive intestinal polypeptide (VIP) was convincingly shown to be involved in the parasympathetic vasodilatation in orofacial areas, such as submandibular glands and lower lip. However, very little is known about the rat masseter muscle. The present study was designed in the rat masseter muscle to assess (1) whether the parasympathetic nerve innervating vessels have VIP immunoreactivities, (2) whether intravenous administration of VIP induces the vasodilatation, and (3) effects of selective VIP receptor antagonist ([4Cl-d-Phe(6), Leu(17)] VIP) in the presence or absence of atropine on the parasympathetic vasodilatation. The VIP immunoreactivities were found at two sites of the parasympathetic otic ganglion and nerve fibres located around vessels. The intravenous administration of VIP induced the vasodilatation, and [4Cl-d-Phe(6), Leu(17)] VIP markedly decreased the vasodilatation evoked by VIP administration. The parasympathetic vasodilatation was not inhibited by [4Cl-d-Phe(6), Leu(17)] VIP. However, treatment with [4Cl-d-Phe(6), Leu(17)] VIP markedly decreased the parasympathetic vasodilatation when [4Cl-d-Phe(6), Leu(17)] VIP was administered together with atropine. These results suggest that (1) VIP exists in the postganglionic parasympathetic nerve innervating the vessels in the masseter muscle, (2) the intravenous administration of VIP induces the vasodilatation in the masseter muscle, and (3) VIP may be involved in the parasympathetic vasodilatation in the masseter muscle when muscarinic cholinergic receptors are deactivated by either atropine or the suppression of the ACh release.

Parasympathetic Vasodilator Fibers in the Orofacial Region

The present report focuses on a review of A) the parasympathetic vasodilator fibers in the orofacial skin, B) the central mechanism by which trigeminal stimulation elicits parasympathetic reflex vasodilatation, and C) the presence of parasympathetic vasodilator fibers in the jaw muscles. A) The parasympathetic neurons, particularly those running as efferents in the glossopharyngeal nerve, were involved in vasodilatation elicited by stimulation of the infra-orbital nerve and the maxillary buccal gingiva. Furthermore, the vasodilator response was not affected by lesion of the pterygopalatine ganglion, suggesting that reflex vasodilatation is mediated via the otic ganglion but not via the pterygopalatine ganglion. B) The trigeminal spinal nucleus is an important bulbar relay for lingual nerve-evoked parasympathetic reflex vasodilatation in the lower lip. C) There are parasympathetic cholinergic and non-cholinergic vasodilator fibers originating from cell bodies in the otic ganglion in the rat masseter muscle, and that these fibers are reflexly activated by trigeminal afferent nerve stimulation. The physiological function of the parasympathetic vasodilator fibers in the orofacial area is unknown. However, it has recently been suggested that the trigeminal system may participate in autonomic and behavioral functions such as feeding and drinking. The present review adds a new facet to the evidence that there is a close link between parasympathetic vasodilator fibers and the trigeminal system in the facial area.

Parasympathetic vasodilator fibers in masseter muscle

Abstract Research into the nervous control of blood flow to the jaw muscles controlling opening and closing of the mouth, especially the masseter muscle, has indicated that sympathetic fibers derived from the superior cervical sympathetic trunk induce vasoconstriction in the masseter muscles of a number of animal species. However, none of these reports has investigated neurally-mediated vasodilatation in the masseter muscle under physiological conditions. The present study was thus designed to examine: 1) whether there are vasodilator fibers in the masseter muscle ; and 2) if there are, to elucidate the neural pathways mediating these responses in urethane-anesthetized rats. Electrical stimulation of the central cut end of the lingual nerve (LN) elicited an intensity- and frequency-dependent increase in blood flow in the masseter muscle (MBF). The MBF increase evoked via LN stimulation was reduced by hexamethonium in a dosedependent manner (1–10 mg/kg). Pretreatment with phentolamine or propranolol at a dose of 100 µ/kg had no effect on the increase in MBF through LN stimulation. Pretreatment with atropine (100 µ/kg) significantly reduced the LN stimulation-induced increase in MBE MBF elevations occurred with electrical stimulation of the trigeminal ganglion, and these increases were significantly reduced via the administration of hexamethonium. Lidocaine microinjection into the trigeminal spinal nucleus or salivatory nuclei caused a significant attenuation of the LN-induced MBF increases. When wheat germ agglutinin-horseradish peroxidase (WGA-HRP) was injected into the masseter muscle, labeled neurons were abundantly observed in the otic ganglion. The present study indicates that there are parasympathetic cholinergic and non-cholinergic vasodilator fibers originating from cell bodies in the otic ganglion in the rat masseter muscle. The MBF increase evoked by activation of the parasympathetic fibers occurred via the trigeminal-mediated reflex, suggesting that this novel parasympathetic vasodilator response may play an important role in the regulation of jaw muscle hemodynamics. This review investigates: A) the presence of vasodilator fibers in masseter muscle ; B) the possible neural pathway leading to vasodilatation mediated by activation of these fibers when the somatic pathway of the trigeminal afferent nerve is electrically stimulated ; and C) the physiological role of neurally-mediated vasodilatation in jaw muscle hemodynamics.