Nociceptive afferent vagal input is enhanced after transection of the aortic depressor nerve.

To test the hypothesis that baroreceptor reflexes are involved in the reduced nociceptive responses associated with hypertension, the effects of acute intravenous doses of serotonin (0.75-144 micrograms/kg) on inhibition of the tail-flick reflex, blood pressure, and heart rate were examined in lightly pentobarbital-anesthetized Sprague-Dawley, Wistar-Kyoto, and spontaneously hypertensive rats before and after bilateral transection of the aortic depressor nerve. Before transection, the ED50s for inhibition of the tail-flick reflex in the three strains of rats were 14, 13, and 44 micrograms/kg, respectively. After bilateral transection of the aortic depressor nerve, all three strains displayed a significant increase in sensitivity toward the serotonin-induced inhibition of the tail-flick reflex (ED50s of 7, 7, and 6 micrograms/kg, respectively). There were no changes in the cardiovascular responses to serotonin after transection of the aortic depressor nerve in Wistar-Kyoto or spontaneously hypertensive rats. In Sprague-Dawley rats, however, the cardio-pulmonary cardiovascular afferent-mediated responses were enhanced. In Sprague-Dawley rats, the nociceptive sensitivity to serotonin was unaltered when administered during either the peak increase or decrease in pressure produced by intravenous phenylephrine or nitroprusside, respectively. These results suggest that 1) afferent fibers within the aortic depressor nerve provide strong tonic inhibitory influences on the noxious information conveyed by the vagus in response to intravenous serotonin and 2) these fibers appear to produce their effects by mechanisms that are unrelated to baroreceptor function.