title: The potential role of prostaglandin D2 in nasal congestion observed in a guinea pig model of allergic rhinitis.
abstract: BACKGROUND
  Allergic rhinitis is the most common allergic disease, displaying the typical nasal symptom of congestion. Prostaglandin D(2) (PGD(2)), a chemical mediator released in large amounts by mast cells upon allergic stimulation in humans, is known to be involved in nasal congestion. However, the mechanism by which this congestion occurs remains unclear.
  
  
  METHODS
  The effect of PGD(2) on the nasal airflow in guinea pigs was measured using a noninvasive approach that avoided any anesthetic effect. Isometric tension of isolated nasal mucosa and the nasal vascular corrosion resin cast technique were used to clarify the area of nasal mucosal vessels affected by PGD(2), and to examine the mechanism of PGD(2)-induced nasal congestion. Moreover, the involvement of second messengers in PGD(2)-induced mucosal relaxation was investigated.
  
  
  RESULTS
  PGD(2) induced an increase in intranasal pressure in a guinea pig model of rhinitis. Additionally, sinusoidal microvessel dilatation appeared around the septum using the vascular corrosion resin cast technique in the nasal mucosa. Moreover, relaxation of the nasal mucosa following stimulation of the prostanoid DP-1 receptor was associated with cAMP levels in the tissue.
  
  
  CONCLUSIONS
  PGD(2)-induced nasal congestion is caused by direct dilatation of the sinusoid vessels through the increase of cAMP levels in the nasal mucosa, demonstrating that the mechanism of PGD(2)-induced nasal congestion is different from other chemical mediators. Consequently, antagonists for the prostanoid DP-1 receptor would be an alternative approach for the relief of nasal congestion. Alternatively, the combined administration with antagonists for other mediators involved in nasal congestion may also be a valuable therapy for allergic rhinitis.
authors.affiliation: United Graduate School of Drug Discovery and Medical Information Sciences, Gifu University, Gifu, Japan.
authors.forename: Go
authors.initials: G
authors.lastname: Takahashi
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Tanaka
authors.forename: Naoko
authors.initials: N
authors.lastname: Higuchi
authors.forename: Minoru
authors.initials: M
authors.lastname: Ikeda
authors.forename: Naoki
authors.initials: N
authors.lastname: Inagaki
authors.forename: Michitaka
authors.initials: M
authors.lastname: Shichijo
mesh_terms: D000818:Animals; D000242:Cyclic AMP / Q000032:analysis; D004195:Disease Models, Animal; D006168:Guinea Pigs; D008297:Male; D009297:Nasal Mucosa / Q000098:blood supply / Q000276:immunology / Q000378:metabolism; D015508:Nasal Obstruction / Q000276:immunology* / Q000378:metabolism; D015230:Prostaglandin D2 / Q000378:metabolism*; D011982:Receptors, Prostaglandin / Q000378:metabolism; D012221:Rhinitis, Allergic, Perennial / Q000276:immunology* / Q000378:metabolism
chemical_list: D011982:Receptors, Prostaglandin; D000242:Cyclic AMP; D015230:Prostaglandin D2