The Role of the Autonomic Nerves in the Control of Nasal Circulation

Lung, Mary A.

doi:10.1159/000109439

Cited by 29 publications

(24 citation statements)

References 19 publications

(28 reference statements)

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“…Experimental selective parasympathetic nerve activation in the nasal mucosa of the cat leads to an increase in nasal secretion and vascular congestion 5. Lung found nasal congestion to be related to a withdrawal of sympathetic discharge rather than to an overactivity of the parasympathetic nerves 6. Thus the nasal hypersecretion and stuffiness in our patient is in agreement with the assumption of a lesion of pericarotid sympathetic nerve fibres after carotid artery dissection.…”

supporting

confidence: 88%

Persisting rhinorrhoea and headache as the initial symptom of bilateral carotid artery dissection

Kahl

Naumann

Toyka

et al. 1999

Journal of Neurology, Neurosurgery & Psychiatry

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supporting

confidence: 88%

Persisting rhinorrhoea and headache as the initial symptom of bilateral carotid artery dissection

Kahl

Naumann

Toyka

et al. 1999

Journal of Neurology, Neurosurgery & Psychiatry

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“…Nasal congestion in vasomotor rhinitis seems to be related to a withdrawal of sympathetic discharge and, at least in part, overactivity of the parasympathetic nerves [1,10]. On the other hand, Masini et al [11] reported that vidian nerve stimulation induces histamine release and vasodilatation in patients with vasomotor rhinitis, and Terrahe [12] suggested a role for mast cell degranulation in vasomotor rhinitis.…”

Section: Discussionmentioning

confidence: 99%

Vasomotor Rhinitis: Clinical Efficacy of Azelastine Nasal Spray in Comparison with Placebo

Géhanno

Deschamps²,

Garay³

et al. 2001

ORL

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The H₁ antagonist azelastine is used in nasal sprays for the treatment of allergic rhinitis, but its therapeutic efficacy in vasomotor rhinitis is unknown. We performed a multicenter randomized double-blind placebo-controlled study of the efficacy and tolerance of azelastine nasal spray in 89 adult patients with vasomotor rhinitis (confirmed by negative Phadiatop). Following a washout period, patients were treated for 15 days with one puff three times daily per nostril of azelastine (n = 44) or placebo (n = 45) nasal spray. Efficacy was evaluated by the reduction in symptomatology and by rhinoscopy. Intent-to-treat analysis revealed better results in the azelastine group for all assessed symptoms; the significance level was reached for nasal obstruction on day 15 (p = 0.042). Using per protocol analysis (in 85 patients complying with the protocol), the significance level was reached for nasal obstruction on day 15 (p = 0.017) and for the percentage of success in rhinorrhea (p = 0.023). In the azelastine group, rhinoscopy examination showed a significantly higher reduction in the inflammatory level and edema of the nasal mucosa (p = 0.03 and 0.02 for VAS on day 15 respectively, per protocol analysis). General efficacy assessment by the physician and the patient was in favor of azelastine (with significance levels <0.01). No drowsiness or serious adverse event was reported, and the frequency of mouth dryness and headaches was similar in the two treatment groups. The present study demonstrates the efficacy of azelastine nasal spray in the treatment of vasomotor rhinitis. The best achieved results were a decrease in nasal obstruction and mucosal edema. Further studies are required to investigate if this therapeutic benefit results from H₁ antagonism or from another, not well-characterized pharmacological action of azelastine.

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“…Concurrent stimulation of the autonomic nerves constricts the capacitance vessels, which signifies that reduced sympathetic activity rather than parasympathetic overactivity may be more important in contributing to nasal congestion. Nonallergic rhinopathies may, therefore, result from loss of sympathetic tone that would normally cause arterial vasoconstriction and decrease in mucosal blood flow [25].…”

Section: Role Of Autonomic Nervous System In Hyperreactivity Of Nasalmentioning

confidence: 99%

Neural Abnormalities in Nonallergic Rhinitis

Bernstein

Singh

2015

Curr Allergy Asthma Rep

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Sensory nerve endings within the airway epithelial cells and the solitary chemoreceptor cells, synapsing with sensory nerves, respond to airborne irritants. Transient receptor potential (TRP) channels (A1 and V1 subtypes, specifically) on these nerve endings initiate local antidromic reflexes resulting in the release of neuropeptides such as substance P and calcitonin G-related peptides. These neuropeptides dilate epithelial submucosal blood vessels and may therefore increase transudation across these vessels resulting in submucosal edema, congestion, and rhinitis. Altered expression or activity of these TRP channels can therefore influence responsiveness to irritants. Besides these pathogenic mechanisms, additional mechanisms such as dysautonomia resulting in diminished sympathetic activity and comparative parasympathetic overactivity have also been suggested as a probable mechanism. Therapeutic effectiveness for this condition has been demonstrated through desensitization of TRPV1 channels with typical agonists such as capsaicin. Other agents effective in treating nonallergic rhinitis (NAR) such as azelastine have been demonstrated to exhibit TRPV1 channel activity through the modulation of Ca(2+) signaling on sensory neurons and in nasal epithelial cells. Roles of antimuscarinic agents such as tiotropium in NAR have been suggested by associations of muscarinic cholinergic receptors with TRPV1. The associations between these channels have also been suggested as mechanisms of airway hyperreactivity in asthma. The concept of the united airway disease hypothesis suggests a significant association between rhinitis and asthma. This concept is supported by the development of late-onset asthma in about 10-40 % of NAR patients who also exhibit a greater severity in their asthma. The factors and mechanisms associating NAR with nonallergic asthma are currently unknown. Nonetheless, free immunoglobulin light chains and microRNA alteration as mediators of these inflammatory conditions may play key roles in this association.

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The Role of the Autonomic Nerves in the Control of Nasal Circulation

Cited by 29 publications

References 19 publications

Persisting rhinorrhoea and headache as the initial symptom of bilateral carotid artery dissection

Persisting rhinorrhoea and headache as the initial symptom of bilateral carotid artery dissection

Vasomotor Rhinitis: Clinical Efficacy of Azelastine Nasal Spray in Comparison with Placebo

Neural Abnormalities in Nonallergic Rhinitis

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