Noxious stimuli activate suprasegmental descending inhibitory controls, providing a negative feedback mechanism to dampen the nociceptive transmission at the level of the spinal cord and the trigeminal system. Orofacial nociception thus, can be regulated by heterotopic application of noxious stimuli, a phenomenon also called diffuse noxious inhibitory controls (DNIC). The present study investigated the effect of DNIC triggered by noxious cold or heat stimulation on trigeminal convergent nociceptive neurons and blood pressure. Extracellular unitary recordings were made from spinal trigeminal nucleus convergent neurons in halothane-anaesthetized rats and the mean arterial blood pressure (MAP) was simultaneously monitored. One hundred and five repetitive (0.66 Hz) electrical shocks were applied to the excitatory receptive field of trigeminal convergent neurons at intensity equal to twice the threshold for nociceptive C-fiber activation. Between the 35th and the 60th stimuli (i. e. for 37.5 s) one animal paw was immersed into hot (48°C) or cold (3 to -12°C) water. All tested units responded to C-fiber stimulation. All were under the influence of DNIC triggered by noxious heat stimulation, which depressed C-fiber-evoked responses by 98 ± 1 %. Such inhibition was accompanied by a significant increase in MAP (23.1 ± 4.5 %). Both the neuronal inhibition and the increase in MAP evoked by noxious heat stimulation were significantly reduced following systemic naloxone (0.4 mg/kg). In contrast, heterotopic noxious cold stimulation had no effect on either neuronal responses or MAP changes. The present results suggest that, contrary to human, in the anaesthetized rat, DNIC can not be triggered by noxious cold stimulation.