Transient receptor potential vanilloid 1 (TRPV1) is involved in pain and neurogenic inflammation. It has recently been found that TRPV1 anatgonism causes hyperthermia in multiple species from mice to humans. In the present study, we investigated whether TRPV1 regulates basal sympathetic nervous system (SNS) activity. C57BL6/J wild-type (WT) mice and TRPV1 knockout (KO) mice were implanted with radio-telemetry probes for measurement of core body temperature. AMG9810 (50 mg/kg) or vehicle (2% DMSO/5% Tween 80/10 ml/kg saline) was injected via the peritoneal route. Adrenoceptor antagonists or vehicle (5 ml/kg saline) was injected s.c. In WT mice, theTRPVl antagonist, AMG9810, caused a significantincrease in body temperature, along with increased noradrenaline concentrations in brown adipose tissue. The hyperthermia was significantly attenuated by the (^-adrenoceptor antagonist propranolol, the mixed a-/p-adrenoceptor antagonist labetalol, and the al-adrenoceptor antagonist prazosin. TRPV1 KO mice have a normal basal body temperature, indicative of developmental compensatory events. Amphetamine (potent sympathomimetic) caused hyperthermia in WT mice, which was reduced in TRPV1 KO mice, suggesting a decreased sympathetic drive in KOs. This study provides new evidence thatTRPVl regulates thermoregulatory pathways, upstream of the SNS.