To assess the role of vasopressin V1a receptor (V1a‐R) in baroreflex control of heart rate (HR) in acute hypovolemia, mean arterial pressure (MAP) and HR were measured in freely moving V1a‐R knockout (KO, n = 6) and wild type mice (WT, n = 5) in 3 conditions; before and after 0.39 ml of blood draw, and after blood recovery. The treatments of blood draw and recovery were accomplished in 4 min each, followed by the 5‐min measurement, respectively. A double lumen catheter was chronically placed in the femoral artery for MAP measurement, drug infusion, and blood draw and recovery. Baroreflex sensitivity of HR (BRS‐HR) was determined by bolus infusion of phenylephrine at the 1.5th min of each condition. MAP (mmHg) was 119 ± 3 in WT and 112 ± 3 in KO before blood draw (P = 0.1), and decreased by 24 ± 4 in KO more than 8 ± 1 in WT after blood draw (P = 0.01). There were no differences in HR (~520 beats/min) before blood draw and the increase after blood draw (~140) between WT and KO (P > 0.3). BRS‐HR (HR/MAP, beats/min/mmHg) was −3.0 ± 0.5 in WT and −6.1 ± 1.9 in KO before blood draw (P = 0.2), and increased to −7.2 ± 1.2 in WT after blood draw (P < 0.05) but, in contrast, decreased to −1.6 ± 0.4 in KO (P < 0.05; KO vs WT, P = 0.001). After blood recovery, BRS‐HR was restored immediately in both groups. Thus, BRS‐HR was enhanced by acute hypovolemia in WT but the response was abolished in KO, suggesting that V1a‐R was involved in enhanced BRS‐HR in acute hypovolemia.
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