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Background: It is known that epinephrine/norepinephrine inhibit acute pain transmission. However, the role of β-adrenoceptors is not clear. Thus, we analyzed if β-1 and/or β-2 adrenoceptors can modulate acute pain transmission by performing in vivo single unit recordings during painful and non-painful peripheral stimulation in rats. Methods: Longitudinal study in which we analyzed seven groups of male rats Wistar: control group (n = 11): saline (0.9 %); EPI group (n = 8): epinephrine 100 mcg; AGOβ1 group (n = 8): dobutamine 125 mcg; ANTβ1 group (n = 9): metoprolol 100 mcg; AGOβ2 group (n = 7): clenbuterol 100 mcg; ANTβ2 group (n = 8): butoxamine 100 mcg; ANTβ1 + EPI group (n = 10): metoprolol 100 mcg + epinephrine 100 mcg. For the statistical analysis we used ANOVA. Results: Epinephrine significantly reduced the basal firing rate (BFR) in 34.1 % (p < 0.05) and also the evoked response by painful stimulation in 56 % (p < 0.05). No change was observed in the evoked response by non-painful stimulation. ANTβ1 was the only β-adrenoceptor acting drug that significantly reduced the evoked response by painful stimulation in 41 % (p < 0.05). None of the other drugs alone affected either the BFR or the evoked response to non-painful or painful stimulation. Conclusion: It is the first time that a β1-adrenoceptor antagonist (metoprolol) probes to be effective in reducing the response to painful stimulation in WDR neurons. [ABSTRACT FROM AUTHOR]