COMPARISON OF THE ACTIONS OF KALLIDIN AND BRADYKININ IN THE SKIN OF NORMAL AND PSORIATIC SUBJECTS

With the recent development of selective drugs acting on the kinin sys tem and the identification of a kallikrein-like enzyme from psoriatic blister fluid, there is now much interest in the possible role of kini ns in psoriasis. We have examined the time-course of the inflammatory (weal and flare) responses to intradermal kallidin (lysbradykinin) and bradykinin in normal volunteers, and have compared the dose-response effect of these agents in normal volunteers and patients with psoriasi s. Initially, normal subjects (n = 5) received coded intradermal injec tions of 50 mu l normal saline containing kallidin or bradykinin (0.1, 0.5, 1.0 and 5.0 mu g). Weal volume, weal area and flare area were ca lculated at 5, 15, 30 and 60 min by measuring two perpendicular diamet ers and change in skinfold thickness. Weal and flare measurements were subsequently made at 15 and 5 min, respectively. Patients with psoria sis (n = 9) and normal subjects (n = 10) were given intradermal inject ions of kallidin (0.1 and 1.0 mu g) and bradykinin (0.1, 0.5 and 1.0 m u g) in clinically normal forearm skin, using histamine and normal sal ine as controls. The dose-response effects of kallidin on weal and fla re responses in human skin were established in the study and compared with those of bradykinin. There was wide inter-individual variability for both agents and, although mean responses to the highest doses of k allidin and bradykinin were decreased in psoriatic skin, no significan t differences were found between the psoriatic and normal group for ka llidin, bradykinin or histamine. Hence, there do not appear to be any obvious altered vascular responses to kallidin or bradykinin in patien ts with psoriasis, despite the fact that kinins may be generated in ps oriatic tissue.