Nasal obstruction is the major symptom in patients with allergic rhinitis, which has become a health problem in Japan. Dilated nasal mucosal blood vessels and enhanced capillary permeability occurs due to the direct action of chemical mediators such as leukotrienes (LTs), thromboxane (TX), prostaglandins (PGs) and platelet-activating factor (PAF). Vasodilatation is also due to neural reflexes through the nucleus and by release of chemical mediators and inflammatory proteins from inflammatory cells. The precise action of such chemical mediators remains unclear, and it appears to be important to determine the direct effect of such mediators and their functions. We studied the nasal mucosal blood vessel response to chemical mediators using an in vitro muscle tension detector and nasal mucosa specimens from guinea pigs and humans. We conducted an in vitro bioassay of responses to LTD
4, TXA
2, PGD
2, and PAF. LTD
4, TXA
2 and PAF showed only a contractile response. The dilation response occurred in human nasal mucosa reacting to PGD
2, suggesting that PGD
2 is involved in nasal obstruction. A specific differences in chemical mediators' response were thus observed, and that of guinea pigs resembled that of humans closely enough to substitute the nasal guinea pig mucosa for that of human beings. Individual receptor antagonists showed antagonism toward corresponding chemical mediators, which are apparently highly involved in the development of allergic rhinitis. It is therefore important to further clarify mediator mechanisms.
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