Mu opioid receptor activation increases body temperature and affects cardiovascular function. In the present study, fentanyl was administered intravenously (iv, 100 µg, 300nmol, per kg) and intracerebroventricularly (icv, 3.4 µg, 10 nmol, in 10 µl) in urethane/chloralose anesthetized, artificially-ventilated rats. Increases in brown adipose tissue sympathetic nerve activity (BAT SNA, peak: +326 % of control), BAT temperature (peak: +0.8 °C), renal SNA (peak: +146 % of control) and heart rate (HR, peak: +32 bpm) produced by iv fentanyl were abolished by pre-mamillary transection of the neuraxis, but were mimicked by icv administration of fentanyl, which also increased arterial pressure (AP, peak: +12 mmHg). Pretreatment with the opioid antagonist, naloxone (icv, 100 nmol in 10 µl), eliminated the icv fentanyl-evoked responses. Microinjection of glycine (0.5M in 60nl) to inhibit local neurons in the rostral raphe pallidus (RPa) selectively reversed the icv fentanyl-evoked increases in BAT SNA and HR, while the fentanyl-evoked excitation in RSNA, the pressor and tachycardic responses were reversed by inhibition of neurons in the rostral ventrolateral medualla (RVLM). Prior inhibition of neurons in the dorsomedial hypothalamus eliminated the icv fentanyl-evoked increases in BAT SNA, BAT temperature and HR, but not those in RSNA or AP. These results indicate that activation of central mu opioid receptors with fentanyl can elicit BAT thermogenesis and cardiovascular stimulation through excitation of the sympathetic outflows to BAT, kidney and heart. Activation of neurons in the rostral RPa and RVLM are respectively essential for the increases in BAT thermogenesis and renal sympathoexcitation induced by activation of central mu opioid receptors. BAT thermogenesis could contribute to fentanyl-evoked hyperthermia, particularly in infants where BAT plays a significant role in thermoregulation.