Activation of the sinoaortic baroreceptor reflex arc induces analgesia: Interactions between cardiovascular and endogenous pain inhibition systems

Abstract

Two experiments examined the view that activation of the sinoaortic baroreceptor reflex arc induces analgesia. Rats were instrumented with carotid artery and jugular vein cannulae for measurement of arterial blood pressure, central venous blood pressure, and heart rate during assays of pain sensitivity using tail-flick responses to radiant heat. In Experiment 1, increases in arterial blood pressure effected by infusion of phenylephrine resulted in profound analgesia that persisted for a 28-min observation period following termination of the infusion. During the phenylephrine infusion period, the degree of analgesia was significantly correlated to the degree of reflex bradycardia, but was not significantly correlated to changes in either arterial or venous blood pressure. In Experiment 2, increases in arterial blood pressure effected by infusion of phenylephrine failed to induce analgesia in rats with bilateral sinoaortic deafferentations, indicating that activation of the sinoaortic baroreceptor reflex arc is required for this form of analgesia. As in Experiment 1, reflex bradycardia, rather than increases in arterial blood pressure, was correlated with analgesia. These outcomes are consistent with the view that systems involved in the regulation of blood pressure are physiologically linked to systems involved in the regulation of pain. The implications of these findings for the etiology of hypertension are discussed.