While experimental baroreceptor stimulation is known to elicit hypoalgesia in healthy individuals, the impact of spontaneous baroreflex sensitivity (BRS) on acute pain responses is not known. We tested for associations between BRS and pain responses in healthy individuals, whether these associations are altered in chronic low back pain (CLBP), and the role of alpha-2 adrenergic (ADRA2) mechanisms in these effects. Twenty-five healthy controls and 21 CLBP subjects completed three acute pain tasks after receiving placebo or an intravenous ADRA2 antagonist (yohimbine hydrochloride, 0.4 mg/kg) across two sessions in counterbalanced order. Resting pre-drug spontaneous BRS was assessed using the sequence method. CLBP subjects displayed lower resting BRS(Down) than controls (p<.05). Drug x BRS(Down) interactions indicated that significant BRS-related hypoalgesia on thermal pain threshold and tolerance was eliminated with yohimbine (p's<.05). Subject Type x BRS(Up) interactions on finger pressure (MPQ-Sensory) and ischemic tasks (MPQ-Sensory, pain threshold, intra-task numeric intensity ratings) indicated that inverse BRS/pain associations in controls (p's<.05) were absent in CLBP subjects. Subject TypexDrug x BRS(Down) interactions on finger pressure MPQ-Sensory and intra-task numeric intensity ratings (p's<.05) indicated that for controls, yohimbine attenuated the significant inverse BRS/pain sensitivity associations noted under placebo. In contrast, CLBP subjects displayed a nonsignificant positive BRS/pain association under placebo, with yohimbine producing an inverse association similar to controls (significant for MPQ-Sensory). Results suggest presence of spontaneous BRS-related hypoalgesia in healthy individuals that is partially mediated by ADRA2 mechanisms, and that CLBP blunts BRS-related hypoalgesia. As a group, the CLBP subjects do not manifest baroreceptor-induced antinociception.