Both the increased nasal vascular permeability and eosinophil accumulation were commonly observed in nasal mucosa with allergic rhinitis. Topical administration of platelet-activating factor (PAF) produced dose-dependent increases in nasal vascular permeability concomitant with the increase in both the histamine and leukotriene C4 (LOC4) concentrations of nasal lavage fluid, in non-sensitized guinea pigs. The selective PAF antagonist CV-3988 inhibited these responses. The PAF-induced nasal vascular permeability was also inhibited by a H1 antagonist (diphenhydramine) and a peptido-LTs antagonist (FPL-55712). However, in ovalbumine (OA)-sensitized guinea pigs, CV-3988 did not affect antigen-induced increase in nasal vascular permeability. Four hours after topical administration of antigen or PAF to OA-sensitized guinea pigs, a marked eosinophil infiltration in the nasal mucosa was noted. This antigen-induced eosinophil infiltration was inhibited by CV-3988. These results suggests that PAF plays a major role in the antigen-induced eosinophil accumulation rather than in the antigen-induced vascular permeability.