The nociceptor sensitization by bradykinin does not depend on sympathetic neurons.

Nociceptive primary afferents develop an increased responsiveness in inflamed tissue. The aim of this neurophysiological investigation was to study the sensitivity changes of cutaneous nociceptors following application of the algesic inflammatory mediator bradykinin and to examine a possible contribution of the sympathetic nervous system. Single unit recordings were obtained in a skin-nerve in vitro preparation from unmyelinated nociceptive afferents supplying the hairy skin of intact or of chronically sympathectomized rats. In preparations from intact skin, mechano-heat-sensitive C-fibres responding to superfusion of the receptive fields with 10 microM bradykinin for 1 min were sensitized to heat stimulation 2 min later. On average, the threshold dropped by 5.0 degrees C, the maximal discharge frequency increased by 34% and the temperature eliciting this peak discharge dropped by 5.6 degrees C. This resulted in a leftward shift and an increased slope of the stimulus-response function indicating sensitization. In surgically sympathectomized animals, 52% of the nociceptive afferents were activated by bradykinin which is not different from normal controls. In sympathectomized animals neither the reduction of the mean threshold (4.6 degrees C) nor the increase of the peak discharge frequency (48%) differed significantly from intact controls. The change of the stimulation-response function following bradykinin application was virtually identical in intact and sympathectomized preparations. Moreover, bradykinin increased the heat discharge of individual fibres by a factor of 2.1 in intact and 1.9 in sympathectomized animals, respectively. In both preparations the increased responsiveness of the nociceptors was short-lived and had resolved 7 min after chemical stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)