Key points Arterial blood pressure rises at the onset of voluntary locomotion, which is probably advantageous for increasing blood flow to contracting muscles without delay. We previously reported in free‐moving mice that the feedback control of arterial blood pressure through peripheral baroreceptors, which was dominant at rest, was suppressed during activation of the cerebral cortex; however, no neurotransmitter for the mechanisms has been identified. Central suppression of the feedback control of arterial blood pressure at the onset of voluntary locomotion was abolished in vasopressin V1a receptor‐deficient mice and by local infusion of a V1a receptor antagonist into the brainstem area, termed the nucleus tractus solitarii, of control mice. Thus, central vasopressin might play an important role as a neurotransmitter in the pressor response at the onset of voluntary locomotion. Abstract  We previously reported that cerebral activation suppressed baroreflex control of heart rate (HR) at the onset of voluntary locomotion. In the present study, we examined whether vasopressin V1a receptors in the brain were involved in these responses by using free‐moving V1a receptor knockout (KO, n= 8), wild‐type mice locally infused with a V1a receptor antagonist into the nucleus tractus solitarii (BLK, n= 8) and control mice (CNT, n= 8). Baroreflex sensitivity (ΔHR/ΔMAP) was determined from HR response (ΔHR) to a spontaneous change in mean arterial pressure (ΔMAP) every 4 s during the total resting period, which was ∼8.7 h, of the 12 h measuring period in the three groups. ΔHR/ΔMAP was determined during the periods when the cross‐correlation function (R(t)) between ΔHR and ΔMAP was significant (P < 0.05). Cerebral activity was determined from the power density ratio of θ to δ wave band (θ/δ) on the electroencephalogram every 4 s. Spontaneous changes in θ/δ were significantly correlated with R(t) during 62 ± 3% of the total resting period in CNT (P < 0.05), but only 38 ± 4% in KO and 47 ± 2% in BLK (vs. CNT, both P < 0.001). When R(t) and ΔHR/ΔMAP were divided into six bins according to the level of θ/δ, both were positively correlated with θ/δ in CNT (both P < 0.001), while neither was correlated in KO or BLK (all P > 0.05). Moreover, the probability that mice started to move after an increase in θ/δ was 24 ± 4% in KO and 24 ± 6% in BLK, markedly lower than 61 ± 5% in CNT (both P < 0.001), with no suppression of the baroreflex control of HR. Thus, central V1a receptors might play an important role in suppressing baroreflex control of HR during cerebral activation at the onset of voluntary locomotion.