Acupuncture potentially offers a non‐pharmacological approach to reduce high blood pressure (BP). Our previous studies have shown that electroacupuncture (EA) attenuates reflex elevation in BP induced by gastric distension (GD) through modulation by several transmitters (e.g., opioids and GABA) in the rostral ventrolateral medulla (rVLM). Although adenosine is released during neuronal activation in the rVLM, its role in acupuncture‐cardiovascular regulation is unknown. Adenosine primarily modulates neuronal function through P1 (specifically, A1, A2, and A3) receptors. Since selective activation of A1 and A2A rVLM receptors respectively induces pressor and depressor responses, we hypothesized that adenosine in the rVLM contributes to EA modulation of sympathoexcitatory reflexes through an A2A but not an A1 adenosine receptor mechanism. Repeated GD every 10 min was performed in Sprague‐Dawley male rats under ketamine and α‐chloralose anesthesia. EA (2 Hz, 0.5 ms, 1–4 mA) was applied at the P5–P6 acupoints, overlying the median nerve, for 30 min after establishing two consistent reflex responses to GDs. We found that repetitive GDs evoked consistent sympathoexcitatory pressor responses. EA (n=5) but not sham‐EA (n=5) at P5–6 (insertion of acupuncture needles into acupoints without electrical stimulation) significantly (P<0.05) attenuated GD‐induced elevations in BPs. EA modulation of sympathoexcitatory cardiovascular reflexes was reversed significantly after rVLM microinjection of SCH 58261 (1 mM in 50 nl; A2A receptor antagonist; n=8; P<0.05), but not by the vehicle (5% dimethylsulfoxide; n=6). Microinjection of DPCPX (3 mM in 50 nl; A1 receptor antagonist; n=4) into the rVLM did not influence EA inhibition of GD‐induced pressor responses. GD‐evoked sympathoexcitatory cardiovascular reflexes, in the absence of EA, were unaltered by administration of SCH 58261 into the rVLM. Neurons labeled with adenosine A2A receptors were co‐localized with neurons stained with tyrosine hydroxylase (i.e., catecholaminergic neurons) in the rVLM. These data suggest that EA modulates sympathoexcitatory cardiovascular responses through an A2A receptor mechanism in the rVLM.Support or Funding InformationNCCIH grant, AT009347.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.