ABSTRACT
Cardiovascular responses to noxious input are well-described, and include elevations in arterial blood pressure and centralization of blood volume; the former being relevant to carotid sinus influences on nociception and the latter being of relevance to vagal influences on nociception. These cardiovascular responses have been traditionally viewed as the requisite hemodynamic adjustments for behaviorally coping with an external threat. The activation of either cervical or subdiaphragmatic vagal afferents evokes antinociception is relatively new, but very well supported. Terminals of primary vagal afferents are located primarily in the caudal third of the nucleus tractus solitarius. The term antinociception is used instead of the term analgesia since this work has been performed in non-humans. Pharmacological, physiological, or high intensity electrical stimulation of vagal afferents results in the production of antinociception, as evidenced by a diminution of either behavioral or spinal neuronal responses evoked by noxious stimuli in non-humans.
