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neurogenic inflammation/potassium
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Activation of large conductance potassium channels inhibits the afferent and efferent function of airway sensory nerves in the guinea pig.
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Sensory nerves play an important role in airway disease by mediating central reflexes such as cough, and local axon reflexes resulting in the peripheral release of neuropeptides. We have tested whether the benzimidazolone compound, NS1619, an opener of large conductance calcium-activated potassium
Capsaicin-evoked CGRP release from rat buccal mucosa: development of a model system for studying trigeminal mechanisms of neurogenic inflammation.
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Many of the physiological hallmarks associated with neurogenic inflammatory processes in cutaneous tissues are similarly present within orofacial structures. Such attributes include the dependence upon capsaicin-sensitive sensory neurons and the involvement of certain inflammatory mediators derived
[Neurogenic inflammation].
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Airway neurogenic inflammation is caused by neuropeptides released from airway sensory nerves, and may be involved in the pathogenesis of asthma. Airway sensory nerves are stimulated by chemical mediators such as bradykinin and leukotrienes, hyperventilation and cigarette smoke. Presynaptic
Neurogenic inflammation and lowering of interstitial fluid pressure in rat trachea is inhibited by alpha-trinositol.
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The effect of alpha-trinositol (D-myoinositol-1,2,6-triphosphate) on edema formation and capillary permeability in neurogenically induced inflammatory edema was investigated in rat trachea. Interstitial fluid pressure (Pif) was studied, since increased negativity of Pif contributes to edema
Potassium channel opener, YM 934, inhibits neurogenic plasma leakage in guinea pig airways.
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The effect of a potassium channel opener, YM 934, on neurogenic airway plasma leakage was examined in anesthetized guinea pigs. Airway plasma leakage was evoked by stimulation of both vagal nerves in the presence of atropine (1 mg/kg, intravenous) and propranolol (1 mg/kg, intravenous), and was
Calcium-activated potassium channels mediate prejunctional inhibition of peripheral sensory nerves.
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Activation of several receptors, including mu-opioid, alpha 2-adrenergic, and neuropeptide Y receptors, inhibits excitatory nonadrenergic noncholinergic (NANC) neural responses in airways, which were mediated by the release of peptides from capsaicin-sensitive sensory nerves. This raises the
Mechanisms of citric acid-induced bronchoconstriction.
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In asthma patients, microaspiration of acid into the lower airways (ie, airway acidification) causes such respiratory responses as cough and bronchoconstriction. The mechanism of bronchoconstriction induced by airway acidification is unknown, although evidence is emerging that increasing proton
Substance P upregulates LTB4 in rat adherent macrophages from granuloma induced by KMnO4.
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Substance P (SP) is an important neuropeptide involved in neurogenic inflammation and most of its pathophysiological functions are mediated through binding to the neurokinin-1 receptor. SP exerts various proinflammatory actions on immune-cells, including macrophages. Several compounds such as
Glial cell line-derived neurotrophic factor family ligands enhance capsaicin-stimulated release of calcitonin gene-related peptide from sensory neurons.
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The glial cell line-derived neurotrophic factor (GDNF) family ligands (GFLs) are a group of peptides that have been implicated as important factors in inflammation, since they are released in increased amounts during inflammation and induce thermal hyperalgesia upon injection. Mouse isolated sensory
[Mechanisms and genetics of migraine].
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Migraine is the most frequent primary headache disorder. It is a neurovascular disorder in which the primary abnormality is thought to be a neuronal excitability underlined by a complex genetic susceptibility. Epidemiogenetic studies have shown that migraine without aura and migraine with aura are
12-Acetoxyhawtriwaic acid lactone, a diterpene from Egletes viscosa, attenuates capsaicin-induced ear edema and hindpaw nociception in mice: possible mechanisms.
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The diterpene, 12-acetoxyhawtriwaic acid lactone (AHAL, tanabalin) isolated from the flower buds of Egletes viscosa Less. (Asteraceae) was evaluated on capsaicin-induced ear edema and hindpaw nociception in mice. AHAL (12.5, 25 and 50 mg/kg, P. O.) significantly attenuated the ear edema response to
An in vitro method to evaluate regulation of neuropeptide release from dental pulp.
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Although pulpal neuropeptides such as calcitonin gene-related peptide and substance P may mediate neurogenic inflammation, little is known about the regulation of neuropeptide release from dental pulp. This article describes an in vitro method for superfusing dental pulp which permits the study of
Evidence for regulatory diversity and auto-regulation at the TAC1 locus in sensory neurones.
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The neuropeptide substance-P (SP) is expressed from the TAC1 gene in sensory neurones where it acts as a key modulator of neurogenic inflammation. The promoter of TAC1 (TAC1prom) plays a central role in the regulation of the TAC1 gene but requires the presence of a second regulatory element; ECR2,
5-HT7 Receptors Are Not Involved in Neuropeptide Release in Primary Cultured Rat Trigeminal Ganglion Neurons.
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Migraine is a common but complex neurological disorder. Its precise mechanisms are not fully understood. Increasing indirect evidence indicates that 5-HT7 receptors may be involved; however, their role remains unknown. Our previous in vivo study showed that selective blockade of 5-HT7 receptors
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