Site-specific autonomic vasomotor responses and their interactions in rat gingiva.

Blood flow in the gingiva, comprising the interdental papilla as well as attached and marginal gingiva, is important for maintaining of gingival function and is modulated by risk factors such as stress that may lead to periodontal disease. Marked blood flow changes mediated by the autonomic (parasympathetic and sympathetic) nervous system may be essential for gingival hemodynamics. However, differences in autonomic vasomotor responses and their functional significance in different parts of the gingiva are unclear. We examined the differences in autonomic vasomotor responses and their interactions in the gingiva of anesthetized rats. Parasympathetic vasodilation evoked by the trigeminal (lingual nerve)-mediated reflex elicited frequency-dependent blood flow increases in gingivae, with the increases being greatest in the interdental papilla. Parasympathetic blood flow increases were significantly reduced by intravenous administration of the atropine and VIP antagonist. The blood flow increase evoked by acetylcholine administration was higher in the interdental papilla than in the attached gingiva, whereas that evoked by VIP agonist administration was greater in the attached gingiva than in the interdental papilla. Activation of the cervical sympathetic nerves decreased gingival blood flow and inhibited parasympathetically induced blood flow increases. Our results suggest that trigeminal-parasympathetic reflex vasodilation 1) is more involved in the regulation of blood flow in the interdental papilla than in the other parts of the gingiva, 2) is mediated by cholinergic (interdental papilla) and VIPergic systems (attached gingiva), and 3) is inhibited by excess sympathetic activity. These results suggest a role in the etiology of periodontal diseases during mental stress.

Differences in the regulatory mechanism of blood flow in the orofacial area mediated by neural and humoral systems.

Marked blood flow (BF) changes mediated by the autonomic neural and humoral systems may be important for orofacial hemodynamics and functions. However, it remains questionable whether differences in the autonomic vasomotor responses mediated by neural and humoral systems exist in the orofacial area. This study examined whether there are differences in changes in the BF and vascular conductance (VC) between the masseter muscle and lower lip mediated by autonomic neural and humoral systems in urethane-anesthetized rats. Electrical stimulation of the central cut end of the lingual nerve elicited BF increases in the masseter (mainly cholinergic) and lower lip (mainly non-cholinergic), accompanied by an increase in arterial blood pressure (ABP), while cervical sympathetic trunk stimulation consistently decreased BF at both sites. The lingual nerve stimulation induced a biphasic change in the VC in the masseter, consisting of an initial decrease and a successive increase. This decrease in VC was positively correlated with changes in ABP and diminished by guanethidine. Cervical vagus nerve stimulation also induced BF increases at both sites; the increases were greater in the masseter than in the lower lip. Adrenal nerve stimulation and isoproterenol administration induced BF increases in the masseter but not in the lower lip. These results indicate that cholinergic parasympathetic-mediated hemodynamics evoked by trigeminal somatosensory inputs are closely related to ABP changes. The sympathetic nervous system, including the sympathoadrenal system and visceral inputs, may be more involved in hemodynamics in the muscles than in epithelial tissues in the orofacial area.

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.

Correction to: Interactions between ß-adrenergic vasodilation and cervical sympathetic nerves are mediated by α2-adrenoceptors in the rat masseter muscle.

The article Interactions between ß-adrenergic vasodilation and cervical sympathetic nerves are mediated by α2-adrenoceptors in the rat masseter muscle, written by Hisayoshi Ishii and Toshiya Sato, was originally published Online First without open access.

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

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 ß-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 ß-adrenergic vasodilation evoked by circulating adrenaline and the cervical sympathetic nerves that is mediated by α2-adrenoceptors in the masseter muscle.

Differences in control of parasympathetic vasodilation between submandibular and sublingual glands in the rat.

We examined blood flow in the submandibular gland (SMGBF) and sublingual gland (SLGBF) during electrical stimulation of the central cut end of the lingual nerve (LN) in the urethane-anesthetized rats using a laser speckle imaging flow meter. LN stimulation elicited intensity- and frequency-dependent SMGBF and SLGBF increases, and the magnitude of the SMGBF increase was higher than that of the SLGBF increase. The increase in both glands was significantly inhibited by intravenous administration of the autonomic cholinergic ganglion blocker hexamethonium. The antimuscarinic agent atropine markedly inhibited the SMGBF increase and partly inhibited the SLGBF increase. The atropine-resistant SLGBF increase was significantly inhibited by infusion of vasoactive intestinal peptide (VIP) receptor antagonist, although administration of VIP receptor antagonist alone had no effect. The recovery time to the basal blood flow level was shorter after LN stimulation than after administration of VIP. However, the recovery time after LN stimulation was significantly delayed by administration of atropine in a dose-dependent manner to the same level as after administration of VIP. Our results indicate that 1) LN stimulation elicits both a parasympathetic SMGBF increase mainly evoked by cholinergic fibers and a parasympathetic SLGBF increase evoked by cholinergic and noncholinergic fibers, and 2) VIP-ergic mechanisms are involved in the noncholinergic SLGBF increase and are activated when muscarinic mechanisms are deactivated.

Parasympathetic reflex vasodilation in the cerebral hemodynamics of rats.

We investigated the role of parasympathetic reflex vasodilation in the regulation of the cerebral hemodynamics, and whether GABAA receptors modulate the response. We examined the effects of activation of the parasympathetic fibers through trigeminal afferent inputs on blood flow in the internal carotid artery (ICABF) and the cerebral blood vessels (rCBF) in parietal cortex in urethane-anesthetized rats. Electrical stimulation of the central cut end of the lingual nerve (LN) elicited intensity- and frequency-dependent increases in ICABF that were independent of changes in external carotid artery blood flow. Increases in ICABF were elicited by LN stimulation regardless of the presence or absence of sympathetic innervation. The ICABF increases evoked by LN stimulation were almost abolished by the intravenous administration of hexamethonium (10 mg kg(-1)) and were reduced significantly by atropine administration (0.1 mg kg(-1)). Although the LN stimulation alone had no significant effect on rCBF, LN stimulation in combination with a blocker of the GABAA receptor pentylenetetrazole increased the rCBF markedly. This increase in rCBF was reduced significantly by the administration of hexamethonium and atropine. These observations indicate that the increases in both ICABF and rCBF are evoked by parasympathetic activation via the trigeminal-mediated reflex. The rCBF increase evoked by LN stimulation is thought to be limited by the GABAA receptors in the central nervous system. These results suggest that the parasympathetic reflex vasodilation and its modulation mediated by GABA receptors within synaptic transmission in the brainstem are involved in the regulation of the cerebral hemodynamics during trigeminal afferent inputs.

GABAB receptors in the NTS mediate the inhibitory effect of trigeminal nociceptive inputs on parasympathetic reflex vasodilation in the rat masseter muscle.

The present study was designed to examine whether trigeminal nociceptive inputs are involved in the modulation of parasympathetic reflex vasodilation in the jaw muscles. This was accomplished by investigating the effects of noxious stimulation to the orofacial area with capsaicin, and by microinjecting GABA(A) and GABA(B) receptor agonists or antagonists into the nucleus of the solitary tract (NTS), on masseter hemodynamics in urethane-anesthetized rats. Electrical stimulation of the central cut end of the cervical vagus nerve (cVN) in sympathectomized animals bilaterally increased blood flow in the masseter muscle (MBF). Increases in MBF evoked by cVN stimulation were markedly reduced following injection of capsaicin into the anterior tongue in the distribution of the lingual nerve or lower lip, but not when injected into the skin of the dorsum of the foot. Intravenous administration of either phentolamine or propranolol had no effect on the inhibitory effects of capsaicin injection on the increases of MBF evoked by cVN stimulation, which were largely abolished by microinjecting the GABA(B) receptor agonist baclofen into the NTS. Microinjection of the GABA(B) receptor antagonist CGP-35348 into the NTS markedly attenuated the capsaicin-induced inhibition of MBF increase evoked by cVN stimulation, while microinjection of the GABA(A) receptor antagonist bicuculline did not. Our results indicate that trigeminal nociceptive inputs inhibit vagal-parasympathetic reflex vasodilation in the masseter muscle and suggest that the activation of GABA(B) rather than GABA(A) receptors underlies the observed inhibition in the NTS.

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.

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.

Role of the spinal trigeminal nucleus in the rat autonomic reflex.

The goal of the present study was to investigate the regional differences between the three subnuclei (oralis, interpolaris, and caudalis) of the spinal trigeminal nucleus (Vsp) in eliciting parasympathetic and sympathetic reflex autonomic responses. We evoked changes in lower lip blood flow (LBF) and systemic arterial blood pressure (SABP) by electrically stimulating these subnuclei in artificially ventilated, urethane-anaesthetised, cervically vago-sympathectomized rats. The LBF increases evoked by electrical stimulation of the Vsp at interpolaris were much larger than those at the sites of the oralis and caudalis. No significant difference in SABP increase was observed by Vsp stimulation between the interpolaris and caudalis, although the SABP increase evoked by electrical stimulation of the oralis was much smaller than in the interpolaris and caudalis. The present findings show that the Vsp at the interpolaris subnucleus of the Vsp participates as a relay in lingual nerve- and Vsp-evoked somato-autonomic reflex.

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 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.

Rapid use-dependent down-regulation of gamma-aminobutyric acid type A receptors in rat mesencephalic trigeminal neurons.

Rundown is ubiquitously seen in response to repetitive activation of receptor or ion channels as a use-dependent down-regulation through various mechanisms. In contrast to AMPA receptors, gamma-aminobutyric acid type A receptor (GABA(A)R) are believed to display no rapid use-dependent down-regulation. We report here a rapid use-dependent down-regulation of GABA(A)R in primary sensory neurons of rat mesencephalic trigeminal nucleus (MTN), which express synaptic GABA(A)Rs in addition to extrasynaptic ones, unlike other primary sensory neurons. When muscimol was repetitively puff-applied to an MTN neuron every 2 min before, during, and after the muscimol bath application for 5 min, both the GABA(A) responses obtained under both current- and voltage-clamp conditions were almost completely depressed during the bath application. However, the former and latter GABA(A) responses recovered to 26% +/- 7% and 36% +/- 7% of their control amplitudes, respectively, 15 min after washout of the bath-applied muscimol. By contrast, when examined in the presence of chelerythrine, a protein kinase C (PKC) inhibitor, together with a stringent chelation of intracellular Ca(2+), the puff responses were almost completely recovered, whereas those were recovered to 40-60% of the control by either chelerythrine or EGTA alone. A phosphatidylinositol 3-kinase inhibitor (PI3K), wortmannin, which blocks various signal transductions, including vesicular trafficking, significantly enhanced the rundown of the puff responses examined every 2 min. These findings indicate that the rundown of GABA(A) response in MTN neurons is mediated by the use-dependent down-regulation of GABA(A)R, which is reversed by PKC inhibition together with intracellular Ca(2+) chelation, while being facilitated by PI3K inhibition.

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.

Inhibitory effects of excess sympathetic activity on parasympathetic vasodilation in the rat masseter muscle.

The present study was designed to examine the effect of sympathetic tonic activity on parasympathetic vasodilation evoked by the trigeminal-mediated reflex in the masseter muscle in urethane-anesthetized rats. Sectioning of the superior cervical sympathetic trunk (CST) ipsilaterally increased the basal level of blood flow in the masseter muscle (MBF). Electrical stimulation of the peripheral cut end of the CST for 2 min using 2-ms pulses ipsilaterally decreased in a dependent manner the intensity (0.5-10 V) and frequency (0.1-5 Hz) of the MBF. The CST stimulation for 2 min at <0.5 Hz with 5 V using 2-ms pulses seems to be comparable with the spontaneous activity in the CST fibers innervating the masseter vasculature, because this stimulation restored the basal level of the MBF to the presectioned values. Parasympathetic vasodilation evoked by electrical stimulation of the central cut end of the lingual nerve in the masseter muscle was markedly reduced by CST stimulation for 2 min with 5 V using 2-ms pulses in a frequency-dependent manner (0.5-5 Hz). Intravenous administration of phentolamine significantly reduced the vasoconstriction induced by CST stimulation in a dose-dependent manner (0.1-1 mg/kg), but pretreatment with either phentolamine or propranolol failed to affect the sympathetic inhibition of the parasympathetic vasodilation. Our results suggest that 1) excess sympathetic activity inhibits parasympathetic vasodilation in the masseter muscle, and 2) alpha- and beta-adrenoceptors do not contribute to sympathetic inhibition of parasympathetic vasodilation, and thus some other types of receptors must be involved in this response.