1. Intraarterial injection of capsaicin (threshold dose 0.3 μg) into the isolated perfused rabbit ear causes a dose-dependent reflex fall in blood pressure by stimulation of chemosensitive nociceptors. 2. Infusion of capsaicin (1 and 10 μg/ml) into the isolated rabbit ear dose-dependently stimulates prostaglandin biosynthesis, equally in innervated and chronically denervated preparations, therefore mainly in extraneuronal tissue. The capsaicin-induced prostaglandin E release is dependent on the presence of extracellular Ca2+. 3. The nociceptive reflex fall in blood pressure induced by i.a. injection of bradykinin is progressively enhanced under infusion of 1 μg/ml capsaicin whereas that induced by acetylcholine is not. Its enhancement is explained by the capsaicin-induced increased amount of prostaglandin E at the nociceptor sites. 4. Infusion of 10 μg/ml capsaicin renders the nociceptors insensitive to effects of bradykinin and acetylcholine. 5. Although the stimulation of nociceptors by capsaicin in a small dose includes the release of prostaglandin E from the surrounding tissue, it cannot be said whether a prostaglandin-mediated mechanism is also involved in the long lasting functional impairment of chemosensitive fibres induced by high doses of capsaicin.