Neural control of human nasal secretion

Baraniuk, James N.

doi:10.1016/0952-0600(91)90035-2

Cited by 41 publications

(30 citation statements)

References 52 publications

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“…Nasal secretions are inhomogeneous fluids revealing considerable intra-and inter-individual variations in amount, composition, physical properties, biological activity and cellular content [19]. These characteristics may change rapidly in response to various stimuli.…”

Section: Discussionmentioning

confidence: 99%

Biological markers in nasal secretions

Riechelmann¹,

Deutschle²,

Friemel³

et al. 2003

Eur Respir J

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Biological markers in nasal secretions provide valuable information on nasal pathophysiology. However, published data on biomarker concentrations in nasal fluids are remarkably inconsistent, and the bias due to different sampling techniques, has not yet been systematically evaluated.Concentrations of various protein were repeatedly determined in nasal secretions of 16 healthy volunteers. The proteins were detected by using: 1) a 2 -macroglobulin as a marker for plasma contamination; 2) lactoferrin as a marker for glandular secretion; 3) lactate dehydrogenase as a marker for tissue injury; and 4) interleukin (IL)-1b, IL-8, tumour necrosis factor-a, and eosinophil cationic protein and tryptase as indicators for tissue inflammation. A total of four different sampling methods, including nasal lavage (NL) and a new polyurethane foam sampler technique (PFST) were employed.Analyte concentrations in NL were approximately10-times lower than in specimens obtained by PFST. Due to the unpredictable dilution during NL, various analytes were below the detection limit of the high sensitivity assays employed. With PFST, concentrations below the detection limit rarely occurred. The specimens did not significantly differ regarding plasma contamination, glandular secretion or tissue injury.The considerable variability of reported analyte concentrations in nasal secretions mainly results from different sampling techniques. To collect nasal secretions, samplers are considered superior to nasal lavage techniques. Eur Respir J 2003; 21: 600-605.

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Section: Discussionmentioning

confidence: 99%

Biological markers in nasal secretions

Riechelmann¹,

Deutschle²,

Friemel³

et al. 2003

Eur Respir J

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“…SP and NKA stimulate mucus secretion from submucosal glands in human airways, both in vitro and in vivo [142,166]. SP is more potent than NKA, indicating the involvement of the NK 1 receptor.…”

Section: Effects Of Tkmentioning

confidence: 99%

Autonomic Innervation of Human Airways: Structure, Function, and Pathophysiology in Asthma

Velden¹,

Hulsmann

1999

Neuroimmunomodulation

126

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The human airways are innervated via efferent and afferent autonomic nerves, which regulate many aspects of airway function. It has been suggested that neural control of the airways may be abnormal in asthmatic patients, and that neurogenic mechanisms may contribute to the pathogenesis and pathophysiology of asthma. In this review, the autonomic innervation of the human airways and possible abnormalities in asthma are discussed. The parasympathetic nervous system is the dominant neuronal pathway in the control of airway smooth muscle tone. Stimulation of cholinergic nerves causes bronchoconstriction, mucus secretion, and bronchial vasodilation. Although abnormalities of the cholinergic innervation have been suggested in asthma, thus far the evidence for cholinergic dysfunction in asthmatic subjects is not convincing. Sympathetic nerves may control tracheobronchial blood vessels, but no innervation of human airway smooth muscle has been demonstrated. β-Adrenergic receptors, however, are abundantly expressed on human airway smooth muscle and activation of these receptors causes bronchodilation. The physiological role of β-adrenergic receptors is unclear and their function seems normal in asthmatic patients. Inhibitory nonadrenergic noncholinergic (NANC) nerves, containing vasoactive intestinal peptide and nitric oxide, may be the only neural bronchodilator pathways in human airways. Although a dysfunction of inhibitory NANC nerves has been proposed in asthma, thus far no differences in inhibitory NANC responses have been found between asthmatics and healthy subjects. Excitatory NANC nerves, extensively studied in animal airways, have also been detected in human airways. In animal studies, stimulation of excitatory NANC nerves causes bronchoconstriction, mucus secretion, vascular hyperpermeability, cough, and vasodilation, a process called ‘neurogenic inflammation’. Recent studies have demonstrated an interaction between the excitatory NANC nervous system and inflammatory cells. Neuropeptides may influence the recruitment, proliferation, and activation of leukocytes. On the other hand, inflammatory cells may modulate the neuronal phenotype and function. The functional relevance of the excitatory NANC nervous system and its interaction with the immune system in asthma still remains to be elucidated.

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“…Hence, sympathetic nerve stim ulation causes constriction of the resistance vessels via the a-adrenergic mechanism and constriction of the capacitance vessels via the a-adrenergic as well as some non-adrenergic and non-cholinergic mechanisms. The sym pathetic nerves supplying the nasal mucosa contain neuropeptide Y and the neuropep tide binding sites are found located on arteri oles and arteriovenous anastomoses [33]. Whether or not this neuropeptide is involved in the sympathetic control of the capacitance vessels as well still awaits further investiga tion.…”

Section: Sympathetic Influencementioning

confidence: 99%

“…Hence, the results suggest that the para sympathetic neurons have a more prominent vasodilatatory action on the posterior venous system. The responses were atropine resis tant, suggesting that the vasodilatation of both resistance and capacitance vessels is via a non-cholinergic mechanism [22], VlP-containing nerves are present near glands and in 183 the walls of blood vessels of the human nasal mucosa [33]. VIP has been shown to cause a potent fall in nasal vascular resistance but lit tle change in nasal airway resistance in the dog [13].…”

Section: Parasympathetic Influencementioning

confidence: 99%

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

Lung¹

1995

Neurosignals

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Patients suffering from allergic or vasomotor rhinitis usually show nasal mucosal hyperaemia, engorgement, hyperrhinorrhoea and obstruction of the nasal airway. The nasal mucosa is drained by two venous systems which are anatomically and functionally separate. The nasal mucosa receives tone discharges from the sympathetic nerves but not from the parasympathetic nerves. Sympathetic nerve stimulation causes constriction of the resistance vessels via the α -adrenergic mechanism and constriction of the capacitance vessels via the α -adrenergic mechanism and some non-adrenergic and non-cholinergic mechanism; the capacitance vessels are under more prominent sympathetic influence than the resistance vessels. Parasympathetic nerve stimulation causes non-cholinergic dilatation of both resistance and capacitance vessels; dilatation is more pronounced in the posterior venous system. Simultaneous optimal stimulation of the autonomic nerves resulted in vasoconstriction, especially of the capacitance vessels. Hence, nasal congestion may be related more to a withdrawal of sympathetic discharge than to an overactivity of the parasympathetic nerves.

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Neural control of human nasal secretion

Cited by 41 publications

References 52 publications

Biological markers in nasal secretions

Biological markers in nasal secretions

Autonomic Innervation of Human Airways: Structure, Function, and Pathophysiology in Asthma

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

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