Synergism between cysteinyl leukotrienes and thromboxane A2 to induce allergic late phase nasal blockage in guinea pigs

Nakanishi, Yasutomo; Nabe, Takeshi; Mizutani, Nobuaki; Takenaka, Hiroshi; Kohno, Shigekatsu

doi:10.1016/j.prostaglandins.2004.07.006

Cited by 9 publications

(4 citation statements)

References 35 publications

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“…In guinea pig models of allergic rhinitis, it has been demonstrated that the concentration of cys-LTs and TXB 2 (a stable TXA 2 metabolite) are elevated in nasal cavity lavage fluid or plasma after antigen challenge [12,13]. These findings suggest that cys-LTs and TXA 2 play an important role in experimental allergic rhinitis of guinea pigs.…”

Section: Introductionmentioning

confidence: 98%

Participation in cysteinyl leukotrienes and thromboxaneA2 in nasal congestion model in Brown Norway rats

Kishi

Nakano

Jiang

et al. 2007

International Immunopharmacology

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Section: Introductionmentioning

confidence: 98%

Participation in cysteinyl leukotrienes and thromboxaneA2 in nasal congestion model in Brown Norway rats

Kishi

Nakano

Jiang

et al. 2007

International Immunopharmacology

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“…Although a combined treatment with pranlukast and seratrodast inhibited late‐phase nasal blockage, the magnitude of inhibition was equal to that elicited by either agent when given alone (Fig. 7) [27]. In contrast, the inhibitory effect of KP‐496, a novel dual antagonist of LTD 4 and TXA 2 receptors, on the nasal blockage in guinea‐pig models of AR was greater than that of pranlukast [28].…”

Section: Introductionmentioning

confidence: 99%

“… Effects of pranlukast, seratrodast, and combined treatment with pranlukast and seratrodast on changes in specific airway resistance after the sixth inhalation challenge with cedar pollen in sensitized guinea‐pigs (reproduced with permission from Nakanishi et al [27]). Pranlukast 30 mg/kg, seratrodast 20 mg/kg, or a combination of both agents was administered 1 h before antigen challenge.…”

Section: Introductionmentioning

confidence: 99%

Mechanism of nasal obstruction in patients with allergic rhinitis

Ichimura

2010

Clin Exp All Rev

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Summary Nasal obstruction is a crucial symptom in allergic rhinitis (AR) patients and may affect the quality of life. It is caused mostly by nasal mucosal obstruction, and to a lesser extent, fluid secretion. Mucosal congestion is primarily a vascular phenomenon comprising vasodilatation of capacitance vessels (cavernous sinus) and oedema formation due to plasma leakage from post‐capillary venules. The nose has a complex microvascular anatomy consisting of capacitance vessels, arteriovenous anastomosis, and subepithelial and periglandular capillaries. Nasal congestion is explained by the effects of local mediators exerting potent vasodilatation or increasing permeability of nasal blood vessels and nerves. Capacitance vessels usually constrict because of constant sympathetic tone. They distend by a variety of stimuli such as loss of continuous sympathetic stimulation on the sinusoids, direct vasodilatation by vasoactive substances, contraction of cushion veins, and compression of venules by distended arteries in the intraosseous bony canals of periosteal space. Although topical application of histamine can cause vasodilatation and oedema, histamine is not likely a major mediator causative of nasal congestion in AR. Nasal vascular dilatation elicited by cysleukotriene 1 (cysLT1) may be induced by nitric oxide produced through cysLT1 receptor activation. Thromboxane A2 may cause capacitance vessel dilatation through a contraction of cushion veins. Potentiation of vasoconstrictor action of steroids has been reported since the 1950s. Glucocorticoids (GCs) have two fundamentally different vascular effects: classic action modifying the transcription of pro‐inflammatory genes and acute non‐genomic action (within minutes) that increases the vasomotor tone. The non‐genomic effect is likely related to binding of GCs to the plasma membrane and inhibition of extraneuronal monoamine transporter on vascular smooth muscle cells, thereby increasing noradrenaline concentrations at α1‐adrenoceptors. Genomic vascular effects include the reduction of vessel density, decrease of hyperperfusion, reduction of inflammatory microvascular hyperpermeability, and decreased influx and activation of inflammatory cells. These effects require hours to manifest themselves physiologically.

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“…6) In guinea pig models of allergic rhinitis, it has been demonstrated that the concentration of TXB 2 , a stable TXA 2 metabolite, is elevated in nasal cavity lavege fluid. 7,8) Accordingly, it is thought that the TXA 2 receptor has an important role in allergic rhinitis.…”

mentioning

confidence: 99%

Prophylactic Effects of the Histamine H1 Receptor Antagonist Epinastine and the Dual Thromboxane A2 Receptor and Chemoattractant Receptor-Homologous Molecule Expressed on Th2 Cells Antagonist Ramatroban on Allergic Rhinitis Model in Mice

Suzuki

Inoue

Yamamoto

et al. 2011

Biological & Pharmaceutical Bulletin

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Synergism between cysteinyl leukotrienes and thromboxane A2 to induce allergic late phase nasal blockage in guinea pigs

Cited by 9 publications

References 35 publications

Participation in cysteinyl leukotrienes and thromboxaneA2 in nasal congestion model in Brown Norway rats

Participation in cysteinyl leukotrienes and thromboxaneA2 in nasal congestion model in Brown Norway rats

Mechanism of nasal obstruction in patients with allergic rhinitis

Prophylactic Effects of the Histamine H1 Receptor Antagonist Epinastine and the Dual Thromboxane A2 Receptor and Chemoattractant Receptor-Homologous Molecule Expressed on Th2 Cells Antagonist Ramatroban on Allergic Rhinitis Model in Mice

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