Comparison of extraoral and intraoral routes of glossopharyngeal nerve block for pain relief in patient with carcinoma tongue: A prospective randomized study.

BACKGROUND AND OBJECTIVE: Glossopharyngeal nerve block (GNB) technique has been used as alternative of treatment of cancer and noncancer pain of the oral cavity. The objective of the study is to compare the two approaches (extraoral and intraoral) of GNB in patients of carcinoma of the tongue in terms of efficacy, duration, and complications. MATERIALS AND METHODS: This was a prospective comparative randomized study over a period of 1 year. Fifty patients of either sex of ASA physical status and 2, between 21 and 70 years of age, suffering from carcinoma of the tongue, were selected. The patients were randomly divided into two groups. Group I received 4 mL of 0.5% bupivacaine combined with 40 mg, of triamcinolonacetonide by extraoral approach of GNB, and Group II received the same amount of drug by intraoral approach of GNB. Hemodynamic parameters, degree of pain relief using visual analog scale (VAS), number of attempts, effect on quality of life (QOL), and complication were noted during the performance of GNB. RESULTS: Demographic profile in both groups was comparable. Rate of complication and number of attempts to complete intervention were higher in Group I, which was found to be statistically significant. However, mean VAS scores in Group I were significantly higher as compared to those in Group II during most of the study period starting from the 1st follow-up at 30 min to the 2nd month postintervention (P < 0.05). No statistically significant difference in mean QOL scores of two groups was observed for the entire study period except at 1 week when mean scores in Group I were higher as compared to those in Group II (P = 0.011). CONCLUSION: The intraoral approach of GNB was better with respect to pain control and improvement in QOL whereas the rate of complication and number of attempts was lower in extraoral approach of GNB.

Proton Pump Inhibitor Ameliorates Taste Disturbance among Patients with Laryngopharyngeal Reflux: A Randomized Controlled Study.

Patients with laryngopharyngeal reflux (LPR) were reported to suffer from hypogeusia that affects quality of life. Proton pump inhibitor (PPI) is a useful drug in the treatment of LPR, but its effect on hypogeusia is not known. We therefore assessed the effects of PPI or a histamine H2 receptor antagonist (H2 blocker) on hypogeusia among patients with LPR. Both PPI and H2 blocker could inhibit acid reflux. LPR was diagnosed with reflux finding score and reflux symptom index. The visual analogue scale (VAS) of taste disturbance symptoms and the gustatory tests were assessed before and 8 weeks after treatment with esomeprazole, a PPI (20 patients, aged 50.0 ± 1.7 years) or famotidine, a H2 blocker (20 patients, aged 47.1 ± 1.8 years). There were no significant differences in VAS scores and recognition thresholds for four basic tastes between the two groups before treatment. Only PPI therapy significantly decreased the VAS scores, suggesting the improvement of taste perception. Moreover, PPI therapy significantly decreased recognition thresholds for bitter taste in the anterior tongue (chorda tympani nerve area) and the thresholds in the posterior tongue (glossopharyngeal nerve area) for salty, sour, and bitter tastes. By contrast, H2-blocker therapy caused no significant changes of thresholds in the anterior tongue, but improved the threshold only for bitter in the posterior tongue, the value of which was however significantly higher than that in PPI group. In conclusion, PPI could ameliorate hypogeusia by improving bitter, salty, and sour tastes among patients with LPR.

Species generalization and differences in Hedgehog pathway regulation of fungiform and circumvallate papilla taste function and somatosensation demonstrated with sonidegib.

Species generalization in the profound, modality-specific effects of Hedgehog pathway inhibition (HPI) in taste organ homeostasis and sensation is shown. With the HPI, cancer drug sonidegib, we demonstrate that the rat taste system, in addition to mouse, is regulated by Hedgehog signaling. After sonidegib treatment for 16-36 days in rat, there is loss of taste buds (TB) in soft palate, in fungiform (FP) and circumvallate papillae (CV), and elimination of taste responses from chorda tympani and glossopharyngeal nerves. The retained innervation in FP and CV during HPI cannot sustain TB. Responses to tactile stimuli are not altered, and temperature responses are reduced only after 28 days treatment, demonstrating modality-specific effects. Rat FP and neural effects are similar to those in mouse whereas TB and neural response effects from the rat CV are much more severe. When recovery is introduced in mouse after prolonged, 48 days HPI, the TB in CV are restored whereas those in FP are not. Overall, Hedgehog signaling regulation is shown to generalize to the rat taste system, and the modality-specific controls in taste organ sensation are affirmed. The reported, debilitating taste disturbances in patients who use HPI drugs can be better understood based on these data.

Postnatal Exposure to Ethanol Increases Its Oral Acceptability to Adolescent Rats.

The aversive flavor of ethanol limits intake by many consumers. We asked whether intermittent consumption of ethanol increases its oral acceptability, using rats as a model system. We focused on adolescent rats because they (like their human counterparts) have a higher risk for alcohol overconsumption than do adult rats following experience with the drug. We measured the impact of ethanol exposure on 1) the oral acceptability of ethanol and surrogates for its bitter (quinine) and sweet (sucrose) flavor components in brief-access lick tests and 2) responses of the glossopharyngeal (GL) taste nerve to oral stimulation with the same chemical stimuli. During the exposure period, the experimental rats had access to chow, water and 10% ethanol every other day for 16 days; the control rats had access to chow and water over the same time period. The experimental rats consumed 7-14 g/day of 10% ethanol across the exposure period. This ethanol consumption significantly increased the oral acceptability of 3%, 6% and 10% ethanol, but had no impact on the oral acceptability of quinine, sucrose or NaCl. The ethanol exposure also diminished responses of the GL nerve to oral stimulation with ethanol, but not quinine, sucrose or NaCl. Taken together, these findings indicate that ethanol consumption increases the oral acceptability of ethanol in adolescent rats and that this increased oral acceptability is mediated, at least in part, by an exposure-induced reduction in responsiveness of the peripheral taste system to ethanol per se, rather than its bitter and sweet flavor components.

Maintenance of Mouse Gustatory Terminal Field Organization Is Disrupted following Selective Removal of Peripheral Sodium Salt Taste Activity at Adulthood.

Neural activity plays a critical role in the development of central circuits in sensory systems. However, the maintenance of these circuits at adulthood is usually not dependent on sensory-elicited neural activity. Recent work in the mouse gustatory system showed that selectively deleting the primary transduction channel for sodium taste, the epithelial sodium channel (ENaC), throughout development dramatically impacted the organization of the central terminal fields of three nerves that carry taste information to the nucleus of the solitary tract. More specifically, deleting ENaCs during development prevented the normal maturation of the fields. The present study was designed to extend these findings by testing the hypothesis that the loss of sodium taste activity impacts the maintenance of the normal adult terminal field organization in male and female mice. To do this, we used an inducible Cre-dependent genetic recombination strategy to delete ENaC function after terminal field maturation occurred. We found that removal of sodium taste neural activity at adulthood resulted in significant reorganization of mature gustatory afferent terminal fields in the nucleus of the solitary tract. Specifically, the chorda tympani and greater superficial petrosal nerve terminal fields were 1.4× and 1.6× larger than age-matched controls, respectively. By contrast, the glossopharyngeal nerve, which is not highly sensitive to sodium taste stimulation, did not undergo terminal field reorganization. These surprising results suggest that gustatory nerve terminal fields remain plastic well into adulthood, which likely impacts central coding of taste information and taste-related behaviors with altered taste experience.SIGNIFICANCE STATEMENT Neural activity plays a major role in the development of sensory circuits in the mammalian brain. However, the importance of sensory-driven activity in maintaining these circuits at adulthood, especially in subcortical structures, appears to be much less. Here, we tested whether the loss of sodium taste activity in adult mice impacts the maintenance of how taste nerves project to the first central relay. We found that specific loss of sodium-elicited taste activity at adulthood produced dramatic and selective reorganization of terminal fields in the brainstem. This demonstrates, for the first time, that taste-elicited activity is necessary for the normal maintenance of central gustatory circuits at adulthood and highlights a level of plasticity not seen in other sensory system subcortical circuits.

Fetal alcohol exposure reduces responsiveness of taste nerves and trigeminal chemosensory neurons to ethanol and its flavor components.

Fetal alcohol exposure (FAE) leads to increased intake of ethanol in adolescent rats and humans. We asked whether these behavioral changes may be mediated in part by changes in responsiveness of the peripheral taste and oral trigeminal systems. We exposed the experimental rats to ethanol in utero by administering ethanol to dams through a liquid diet; we exposed the control rats to an isocaloric and isonutritive liquid diet. To assess taste responsiveness, we recorded responses of the chorda tympani (CT) and glossopharyngeal (GL) nerves to lingual stimulation with ethanol, quinine, sucrose, and NaCl. To assess trigeminal responsiveness, we measured changes in calcium levels of isolated trigeminal ganglion (TG) neurons during stimulation with ethanol, capsaicin, mustard oil, and KCl. Compared with adolescent control rats, the adolescent experimental rats exhibited diminished CT nerve responses to ethanol, quinine, and sucrose and GL nerve responses to quinine and sucrose. The reductions in taste responsiveness persisted into adulthood for quinine but not for any of the other stimuli. Adolescent experimental rats also exhibited reduced TG neuron responses to ethanol, capsaicin, and mustard oil. The lack of change in responsiveness of the taste nerves to NaCl and the TG neurons to KCl indicates that FAE altered only a subset of the response pathways within each chemosensory system. We propose that FAE reprograms development of the peripheral taste and trigeminal systems in ways that reduce their responsiveness to ethanol and surrogates for its pleasant (i.e., sweet) and unpleasant (i.e., bitterness, oral burning) flavor attributes.NEW & NOTEWORTHY Pregnant mothers are advised to avoid alcohol. This is because even small amounts of alcohol can alter fetal brain development and increase the risk of adolescent alcohol abuse. We asked how fetal alcohol exposure (FAE) produces the latter effect in adolescent rats by measuring responsiveness of taste nerves and trigeminal chemosensory neurons. We found that FAE substantially reduced taste and trigeminal responsiveness to ethanol and its flavor components.

Selective Deletion of Sodium Salt Taste during Development Leads to Expanded Terminal Fields of Gustatory Nerves in the Adult Mouse Nucleus of the Solitary Tract.

Neuronal activity plays a key role in the development of sensory circuits in the mammalian brain. In the gustatory system, experimental manipulations now exist, through genetic manipulations of specific taste transduction processes, to examine how specific taste qualities (i.e., basic tastes) impact the functional and structural development of gustatory circuits. Here, we used a mouse knock-out model in which the transduction component used to discriminate sodium salts from other taste stimuli was deleted in taste bud cells throughout development. We used this model to test the hypothesis that the lack of activity elicited by sodium salt taste impacts the terminal field organization of nerves that carry taste information from taste buds to the nucleus of the solitary tract (NST) in the medulla. The glossopharyngeal, chorda tympani, and greater superficial petrosal nerves were labeled to examine their terminal fields in adult control mice and in adult mice in which the α-subunit of the epithelial sodium channel was conditionally deleted in taste buds (αENaC knockout). The terminal fields of all three nerves in the NST were up to 2.7 times greater in αENaC knock-out mice compared with the respective field volumes in control mice. The shapes of the fields were similar between the two groups; however, the density and spread of labels were greater in αENaC knock-out mice. Overall, our results show that disruption of the afferent taste signal to sodium salts disrupts the normal age-dependent "pruning" of all terminal fields, which could lead to alterations in sensory coding and taste-related behaviors. SIGNIFICANCE STATEMENT: Neural activity plays a major role in the development of sensory circuits in the mammalian brain. To date, there has been no direct test of whether taste-elicited neural activity has a role in shaping central gustatory circuits. However, recently developed genetic tools now allow an assessment of how specific taste stimuli, in this case sodium salt taste, play a role in the maturation of the terminal fields in the mouse brainstem. We found that the specific deletion of sodium salt taste during development produced terminal fields in adults that were dramatically larger than in control mice, demonstrating for the first time that sodium salt taste-elicited activity is necessary for the normal maturation of gustatory inputs into the brain.

Inhibitory control of ascending glutamatergic projections to the lamprey respiratory rhythm generator.

Neurons within the vagal motoneuron region of the lamprey have been shown to modulate respiratory activity via ascending excitatory projections to the paratrigeminal respiratory group (pTRG), the proposed respiratory rhythm generator. The present study was performed on in vitro brainstem preparations of the lamprey to provide a characterization of ascending projections within the whole respiratory motoneuron column with regard to the distribution of neurons projecting to the pTRG and related neurochemical markers. Injections of Neurobiotin were performed into the pTRG and the presence of glutamate, GABA and glycine immunoreactivity was investigated by double-labeling experiments. Interestingly, retrogradely labeled neurons were found not only in the vagal region, but also in the facial and glossopharyngeal motoneuron regions. They were also present within the sensory octavolateral area (OLA). The results show for the first time that neurons projecting to the pTRG are immunoreactive for glutamate, surrounded by GABA-immunoreactive structures and associated with the presence of glycinergic cells. Consistently, GABAA or glycine receptor blockade within the investigated regions increased the respiratory frequency. Furthermore, microinjections of agonists and antagonists of ionotropic glutamate receptors and of the GABAA receptor agonist muscimol showed that OLA neurons do not contribute to respiratory rhythm generation. The results provide evidence that glutamatergic ascending pathways to the pTRG are subject to a potent inhibitory control and suggest that disinhibition is one important mechanism subserving their function. The general characteristics of inhibitory control involved in rhythmic activities, such as respiration, appear to be highly conserved throughout vertebrate evolution.

Sodium aspartate as a specific enhancer of salty taste perception-sodium aspartate is a possible candidate to decrease excessive intake of dietary salt.

The excessive intake of dietary salt is a global issue in health. Attempts have been made to address this issue, including the development of salt substitutes. Yet, none of these substances are currently in wide use, because of their weak saltiness. The purpose of this study was to assess the effects of sodium aspartate (Asp-Na) on salty taste perception using the bullfrog glossopharyngeal nerve response and human sensory tests. When added to the mixture of NaCl and KCl, Asp-Na significantly enhanced the glossopharyngeal nerve response to the mixture by 1.6-fold compared to control. Asp-Na did not enhance the response to NaCl, nor did Asp-Na enhance the response to sour, bitter, or umami stimuli. The optimal concentration for Asp-Na to enhance the salt mixture was 1.7mM. The largest enhancement was induced when NaCl and KCl were mixed at equimolar concentrations. Asp-Na significantly suppressed the glossopharyngeal nerve response to quinine hydrochloride, which suggests that bitterness of KCl is suppressed by Asp-Na. The salty taste enhancing effect of Asp-Na was also confirmed with human sensory tests. The present results suggested that the mixture of NaCl and KCl containing Asp-Na can be used as a salt substitute. In addition to demonstrating that Asp-Na enhanced salt taste responses in an experimental animal and human, our findings provide clues to identify the elusive salty taste receptors.

Managing endodontic patients with severe gag reflex by glossopharyngeal nerve block technique.

INTRODUCTION: Gagging is a protective reflex, but when the gag reflex becomes abnormally active, it poses a difficulty for the dentist because it hinders all aspects of dental procedures including diagnosis, radiography, and any form of active procedure. METHODS: In this case report, to overcome this difficulty the authors used a glossopharyngeal nerve block technique that is used by anesthetists and otolaryngologists, but its endodontic use has gone previously unreported. RESULTS: Response to gag reflex decreases after successful glossopharyngeal nerve block. CONCLUSIONS: The glossopharyngeal nerve block technique is a relatively safe, simple, and easy to master technique as compared with general anesthesia for treating a patient with an exaggerated gag reflex. The glossopharyngeal nerve block technique may be used in dental procedures in patients with an exaggerated gag reflex or when performing procedures in the posterior aspect of the mouth. Due caution should be exercised to prevent inadvertent intravascular administration of local anesthetic when using this procedure.

Peripheral glycerol injection: an alternative treatment of children with glossopharyngeal neuralgia.

Glossopharyngeal neuralgia is much less common in children and more difficult to relief its pain symptoms than the adults. We report an experience with peripheral glycerol injection for the control of pain in eight sick children with glossopharyngeal neuralgia. At the latest follow-up, 5 cases had a complete pain-free result after the treatment. There were two sick children who were recurred within three months, of which one child was respond to additional injections. It is concluded that the peripheral glycerol injection is safe and effective in the control of pain symptom among the children with glossopharyngeal neuralgia.

Purinergic stimulation of carotid body efferent glossopharyngeal neurones increases intracellular Ca2+ and nitric oxide production.

The mammalian carotid body (CB) is a peripheral chemosensory organ that controls ventilation and is innervated by both afferent and efferent nerve fibres. The afferent pathway is stimulated by chemoexcitants, such as hypoxia, hypercapnia and acidosis. The efferent pathway causes inhibition of the sensory discharge via release of NO that originates mainly from neuronal nitric oxide synthase (nNOS)-positive autonomic neurones within the glossopharyngeal nerve (GPN). Recent studies in the rat indicate that these inhibitory GPN neurones and their processes express purinergic P2X receptors and can be activated by ATP, a key excitatory CB neurotransmitter. Here we tested the hypothesis that purinergic agonists stimulate a rise in [Ca(2+)]i, leading to nNOS activation and NO production in isolated GPN neurones, using the fluorescent probes fura-2 and 4-amino-5-methylamino-2',7'-difluorofluorescein diacetate (DAF-FM DA), respectively. ATP caused a dose-dependent increase in [Ca(2+)]i in GPN neurones (EC50 ≈ 1.92 µm) that was markedly inhibited by a combination of 100 µm suramin (a non-specific P2X blocker) and 100 nm Brilliant Blue G (a selective P2X7 blocker). ATP also stimulated NO production in GPN neurones, as revealed by an increase in DAF fluorescence; this NO signal was inhibited by purinergic blockers, chelators of extracellular Ca(2+), the nNOS inhibitor l-NAME and the NO scavenger carboxy-PTIO. The P2X2/3 and P2X7 agonists α,ß,-methylene ATP and benzoyl ATP mimicked the effects of ATP. Taken together, these data indicate that ATP may contribute to negative feedback inhibition of CB sensory discharge via purinergic stimulation of NO production in efferent fibres.

Water drinking-related muscle contraction induces the pressor response via mechanoreceptors in conscious rats.

Water drinking is known to induce the pressor response. The efferent pathway in this response involves sympathoexcitation, because the pressor response was completely abolished by ganglionic blockade or an α(1)-adrenergic antagonist. However, the afferent pathway in this response has not been identified. In the present study, we hypothesized that water itself stimulates the upper digestive tract to induce the pressor response, and/or drinking-related muscle contraction induces the pressor response via mechanoreceptors. To examine this hypothesis, we evaluated the pressor response induced by spontaneous or passive water drinking in conscious rats. Since the baroreflex modulates and obscures the pressor response, the experiments were conducted using rats with sinoaortic denervation. The pressor response was not suppressed by 1) transient oral surface anesthesia using lidocaine, 2) bilateral denervation of the glossopharyngeal nerve and sensory branch of the superior laryngeal nerve, or 3) denervation of the tunica adventitia in the esophagus. However, the pressor response was significantly suppressed (by -52%) by intravenous gadolinium chloride administration. Electrical stimulation of the hypoglossal nerve induced the pressor response, which was significantly suppressed (by -57%) by intravenous gadolinium chloride administration and completely abolished by severing the distal end of this nerve. These results indicate that afferent signals from mechanoreceptors in drinking-related muscles are involved in the water drinking-induced pressor response.

Efferent fibers innervate gustatory and mechanosensitive afferent fibers in frog fungiform papillae.

A possibility of efferent innervation of gustatory and mechanosensitive afferent fiber endings was studied in frog fungiform papillae with a suction electrode. The amplitude of antidromic impulses in a papillary afferent fiber induced by antidromically stimulating an afferent fiber of glossopharyngeal nerve (GPN) with low voltage pulses was inhibited for 40 s after the parasympathetic efferent fibers of GPN were stimulated orthodromically with high voltage pulses at 30 Hz for 10 s. This implies that electrical positivity of the outer surface of papillary afferent membrane was reduced by the efferent fiber-induced excitatory postsynaptic potential. The inhibition of afferent responses in the papillae was blocked by substance P receptor blocker, L-703,606, indicating that substance P is probably released from the efferent fiber terminals. Slow negative synaptic potential, which corresponded to a slow depolarizing synaptic potential, was extracellularly induced in papillary afferent terminals for 45 s by stimulating the parasympathetic efferent fibers of GPN with high voltage pulses at 30 Hz for 10 s. This synaptic potential was also blocked by L-703,606. These data indicate that papillary afferent fiber endings are innervated by parasympathetic efferent fibers.

Major differences in the proportion of amino acid fiber types transmitting taste information from oral and extraoral regions in the channel catfish.

The present study investigates for the first time in any teleost the amino acid specificity and sensitivity of single glossopharyngeal (cranial nerve IX) fibers that innervate taste buds within the oropharyngeal cavity. These results are contrasted with similar data obtained from facial (cranial nerve VII) fibers that innervate extraoral taste buds. The major finding is that functional differences are clearly evident between taste fibers of these two cranial nerves. Catfish possess the most extensive distribution of taste buds found in vertebrates. Taste buds on the external body surface are exclusively innervated by VII, whereas IX, along with the vagus (X), innervate the vast majority of taste buds within the oropharyngeal cavity. Responses to the l-isomers of alanine (Ala), arginine (Arg), and proline (Pro), the three most stimulatory amino acids that bind to independent taste receptors, were obtained from 90 single VII and 64 single IX taste fibers. This study confirmed a previous investigation that the amino acid responsive VII fibers consist of two major groups, the Ala and Arg clusters containing taste fibers having thresholds in the ηM range. In contrast, the present study indicates the amino acid responsive IX taste system is dominated by taste fibers responsive to Pro and to Pro and Arg, respectively, has a reduced percentage of Ala fibers, and is less sensitive than VII. The present electrophysiological results are consistent with previous experiments, indicating that the extraoral taste system is essential for appetitive behavior, whereas oropharyngeal taste buds are critical for consummatory behavior.

The role of transient receptor potential vanilloid-1 on neural responses to acids by the chorda tympani, glossopharyngeal and superior laryngeal nerves in mice.

The transient receptor potential vanilloid-1 (TRPV1) receptor acts as a polymodal nociceptor activated by capsaicin, heat, and acid. TRPV1, which is expressed in sensory neurons innervating the oral cavity, is associated with an oral burning sensation in response to spicy food containing capsaicin. However, little is known about the involvement of TRPV1 in responses to acid stimuli in either the gustatory system or the general somatosensory innervation of the oropharynx. To test this possibility, we recorded electrophysiological responses to several acids (acetic acid, citric acid and HCl) and other taste stimuli from the mouse chorda tympani, glossopharyngeal and superior laryngeal nerves, and compared potential effects of iodo-resiniferatoxin (I-RTX), a potent TRPV1 antagonist, on chemical responses of the three nerves. The results indicated that in the chorda tympani nerve, I-RTX (1-100 nM) did not affect responses to acids, sucrose and quinine HCl, but reduced responses to NaCl (I-RTX at concentrations of 10 and 100 nM) and KCl and NH(4)Cl (100 nM). In contrast, in the glossopharyngeal nerve, I-RTX significantly suppressed responses to all acids and salts, but not to sucrose and quinine HCl. Responses to acetic acid were suppressed by I-RTX even at 0.1 nM concentration. The superior laryngeal nerve responded in a concentration-dependent manner to acetic acid, citric acid, HCl, KCl, NH(4)Cl and monosodium l-glutamate. The responses to acetic acid, but not to the other stimuli, were significantly inhibited by I-RTX. These results suggested that TRPV1 may be involved in the mechanism for responses to acids presented to the posterior oral cavity and larynx. This high degree of responsiveness to acetic acid may account for the oral burning sensation, known as a flavor characteristic of vinegar.

Time course of alterations in pre- and post-synaptic chemoreceptor function during developmental hyperoxia.

Postnatal hyperoxia exposure reduces the carotid body response to acute hypoxia and produces a long-lasting impairment of the ventilatory response to hypoxia. The present work investigated the time course of pre- and post-synaptic alterations following exposure to hyperoxia (Fl(O2) = 0.6) for 1, 3, 5, 8 and 14 days (d) starting at postnatal day 7 (P7) as compared to age-matched controls. Hyperoxia exposure for 1d enhanced the nerve response and glomus cell calcium response to acute hypoxia, but exposure for 3-5d caused a significant reduction in both. Hypoxia-induced catecholamine release and nerve conduction velocity were significantly decreased by 5d hyperoxia. We conclude that hyperoxia exerts pre-synaptic (glomus cell calcium and secretory responses) and post-synaptic (afferent nerve excitability) actions to initially enhance and then reduce the chemoreceptor response to acute hypoxia. The parallel changes in glomus cell calcium response and nerve response suggest causality between the two and that environmental hyperoxia can affect the coupling between acute hypoxia and glomus cell calcium regulation.

Antihypertensive role of glossopharyngeal nerve stimulation by nifedipine using as calcium channel blocking agent in hypertension: an experimental study.

Nifedipine is a therapeutic drug in acute attacks of hypertension because of its rapid absorption from oral mucosa. Taste receptors are innervated by glossopharyngeal nerves (GPN) as well as by facial and vagal nerves. Sensory neurons of the GPNs are localised in the petrous ganglion (PG). Transection of the taste sensitive GPN fibres causes taste bud and PG degeneration and spontaneous hypertension. In this study, the role of chemical stimulation of the taste buds of the GPN by nifedipine and its role in treatment of hypertension were investigated in rabbits. Nifedipine was dropped sublingually (20 mg) for 4 days in the study group, followed by measuring blood pressures again. Then, the lingual branches of GPNs were cut. One month later, blood pressures were measured for 4 days. All animals were sacrificed humanely at the end of the experiment, and normal and degenerated neuron densities in the petrosal ganglions were enumerated stereologically. The antihypertensive effect of nifedipine decreased after GPNs denervation, in accordance with the increase of degenerated neurons in the PG. The chemical stimulation of taste buds of the GPNs by nifedipine may be an important effect of nifedipine application in addition to its calcium channel blocking effect. The rapid decrease in blood pressure following sublingual use of nifedipine may also result from the direct stimulation of taste buds innervated by the GPNs.