While it is generally assumed that nociceptor sensitization underlies peripheral hyperalgesia, there is disagreement regarding the ability of inflammatory mediators to sensitize nociceptors to mechanical stimuli. In this in vivo electrophysiological study, mechanical threshold and response to sustained threshold and sustained suprathreshold mechanical stimuli were measured before and after intradermal administration of prostaglandin E2 (PGE2) into the receptive field of cutaneous C-fiber nociceptors in the rat. PGE2 produced a decrease in mechanical threshold and an increase in response to sustained threshold but not sustained suprathreshold mechanical stimulation. These data suggest that while inflammatory mediators produce a decrease in mechanical threshold and/or an increase in number of action potentials to sustained threshold stimuli, they do not increase the maximal response to mechanical stimuli in C-fiber nociceptors.