It has been reported that systemic injection of arginine vasopressin (AVP) induces a drop in body core temperature (T_c), but little is known about the mechanisms involved. Since glutamate is an important excitatory neurotransmitter involved in a number of thermoregulatory actions, in the present study, we tested the hypothesis that glutamate plays a role in systemic AVP-induced hypothermia. Wistar rats were pretreated intracerebroventricularly with kynurenic acid, an antagonist of L-glutamate ionotropic receptors, -methyl-4-carboxyphenylglycine (MCPG), an antagonist of L-glutamate metabotropic receptors, or saline 15 min before intravenous (i.v.) injection of AVP (2 µg/kg) or saline. T_c, brown adipose tissue (BAT) temperature (T_BAT), blood pressure (BP), heart rate (HR) and tail skin temperature (T_skin) were measured continuously. Intracerebroventricular (i.c.v.) administration of saline followed by i.v. AVP caused a significant drop in T_c brought about by a reduction in thermogenesis and an increase in heat loss through the tail. I.c.v. MCPG treatment did not affect the fall in T_c induced by AVP. I.c.v. treatment with kynurenic acid abolished AVP-induced hypothermia but did not affect the AVP-evoked rise in BP or the drop in HR and T_BAT. Heat loss through the tail was significantly reduced in animals injected with AVP and pretrated with kynurenic acid. These data indicate that ionotropic receptors of L-glutamate in the CNS participate in peripheral AVP-induced hypothermia by affecting heat loss through the tail.