Budesonide inhibits plasma extravasation induced by capsaicin and by substance P in the rat nasal mucosa

  title={Budesonide inhibits plasma extravasation induced by capsaicin and by substance P in the rat nasal mucosa},
  author={Elena Bacci and Claude P. Bertrand and Pierangelo Geppetti and Jonathan Baker and Jay A. Nadel and Lauri A. Laitinen and G{\"o}ran Petersson},
  journal={Regulatory Peptides},

The inhibition of neurogenic inflammation.

Glucocorticoid Inhibition of Neuropathic Hyperalgesia and Spinal Fos Expression

Chronic continuous infusion of the glucocorticoid, methylprednisolone, relieved pain in a rodent model of nerve injury, and this effect persisted after discontinuing the drug.

Medicament renfermant un budesonide destine a ameliorer la resorption intestinale des fluides en particulier dans des conditions post-operatoires

L'invention a pour objet l'utilisation d'un budesonide dans le but de traiter les etats provoques par une resorption intestinale reduite des fluides, en particulier les etats post-operatoires



Neurogenic plasma extravasation in the rat nasal mucosa is potentiated by peptidase inhibitors.

It is concluded that neurogenic inflammation in the rat nasal mucosa is greatest in the naso- and maxilloturbinates and can be modulated by NEP-24.11 and, to a lesser extent, by ACE.

Glucocorticoids inhibit neurogenic plasma extravasation and prevent virus-potentiated extravasation in the rat trachea.

Dexamethasone reduced, in a dose-dependent fashion, the magnitude of plasma extravasation produced in the rat trachea by capsaicin and substance P, and prevented the potentiation of neurogenic plasmaExtravasation usually present after 5 d of Sendai virus respiratory infection.

Nasal effects of bradykinin and capsaicin: influence on plasma protein leakage and role of sensory neurons.

It is suggested that bradykinin-induced nasal discomfort and rhinorrhea are neurally mediated, whereas the effects on nasal airways resistance and plasma protein exudation are due to a direct vascular action.

Capsaicin Sensitive Afferents Contribute to Acute Airway Edema following Tracheal Instillation of Hydrochloric Acid or Gastric Juice in the Rat

The formation of acute edema in the tracheobronchial mucosa following local instillation of hydrochloric acid or gastric juice was studied in rats. Protein extravasation using the Evans blue

Effect of intranasal capsaicin on symptoms and mediator release.

Capsaicin causes nasal symptoms and glandular stimulation without evidence of increased vascular permeability or mast cell activation, and ETS-rhinorrhea symptoms in humans appear related to c-fiber stimulation.

Intranasally administered budesonide, a glucocorticoid, does not exert its clinical effect through vasoconstriction.

The possibility of a similar 'vasoconstrictor' phenomenon existing in the upper airway mucosa, which might offer one explanation for the clinically beneficial effect of topical glucocorticosteroid preparations in the treatment of allergic and non-allergic rhinitis, is explored.

Increased vascular permeability in rat nasal mucosa induced by substance P and stimulation of capsaicin-sensitive trigeminal neurons.

Chemogenic irritation of the nasal mucosa by capsaicin induces edema probably via a local axon reflex inducing release of SP, which may be involved in the pathogenesis of nasal congestion seen in various types of rhinitis.

Effect of a Topical Glucocorticoid, Budesonide, on Nasal Mucosal Blood Flow as Measured with 133 Xe Wash‐Out Technique

It seems likely that a more complex activity than vasoconstriction is responsible for the clinical effect in the treatment of nasal disorders, and further research is required in order to clarify this issue.

Clinical and inflammatory responses to exogenous tachykinins in allergic rhinitis.

The order of activity [substance P much greater than neurokinin A greater than substance P(1-9) = saline] indicates an NK1 receptor-mediated mechanism inducing local vasodilation inducing allergic rhinitis.

Role of neutral endopeptidase and kininase II on substance P-induced increase in nasal obstruction in patients with allergic rhinitis.

We studied the role of neutral endopeptidase (NEP) and kininase II (angiotensin-converting enzyme; ACE) in the modulation of exogenous substance P (SP)-induced nasal response in normal subjects and