1. The effects of stimulating the peripheral end of the right splanchnic nerve in the presence of naloxone (2 mg kg-1) have been investigated in conscious 3 to 6-week-old calves. 2. Mean aortic blood pressure rose to significantly higher levels during splanchnic stimulation in bursts at 40 Hz for 1 s at 10 s intervals than it did during stimulation at the corresponding continuous frequency (4 Hz). Furthermore, naloxone significantly reduced the fall in mean vascular resistance in response to both patterns of stimulation. 3. The output of catecholamines from the adrenal gland, together with the proportion of noradrenaline released, was significantly enhanced by stimulating the splanchnic nerves in bursts in animals pre-treated with naloxone and the proportion of noradrenaline released also increased. In both cases the output of adrenaline and noradrenaline was within the same range as that reported previously in normal control animals. 4. Naloxone significantly increased the amounts of enkephalin-like immunoreactivity and corticotrophin-releasing factor (CRF)-like immunoreactivity released from the adrenal gland in response to splanchnic nerve stimulation and raised the proportion of total to free met5-enkephalin that was secreted. 5. Naloxone also inhibited the rise in plasma adrenocorticotrophic hormone (ACTH) concentration during continuous stimulation at 4 Hz, but not during stimulation at 40 Hz in bursts. Under these latter conditions the output of cortisol apparently directly from the adrenal gland was inhibited. The finding that splanchnic nerve stimulation can potentiate the output of cortisol in response to ACTH was confirmed. 6. These results provide evidence that release of enkephalins and of CRF from the adrenal is inhibited by activating opioid receptors within the gland itself.