Angiotensin II (AII), arginine vasopressin (AVP) and prolactin (PRL) were measured by radioimmunoassay in plasma and cerebrospinal fluid (CSF) in concurrent daily samples from conscious unrestrained steers. Packed cell volume, [Na+] and osmolality were also measured from these samples. Salt appetite was assessed during a 5-min daily session of operant conditioning. Food and water was always available. Unilateral parotid duct fistulation was effected under xylazine analgesia and halothane/Ch anaesthesia. To prevent a sodium deficit developing from loss of [Na+] in the extruded saliva, 0.3 M NaHC03 was available ad libitum so that each animal could ingest sufficiently to balance the salivary loss. A week later epidural cannulae were implanted in the cisternae magna using the same anaesthesia. Three days afterwards when the saliva [Na] was 78 mmol/l, the 0.3-M NaHCO3 supplement was withdrawn for 7 days so that sodium deficiency developed to a degree which evoked salt appetite. When the NaHC03 supplement was restored ad libitum, all aspects of [Na+] deficiency and salt appetite were completely ameliorated within 2–3 days. Packed cell volume increased and body weight decreased (p < 0.05) during depletion, but rapidly returned to normal on day 2 of repletion. Both plasma and CSF osmolality were reduced during depletion as were plasma [Na+] (p < 0.01) and CSF [Na+] (p < 0.001). From a basal value of 64.7 ± 9.35 fmol/ml on day 0, plasma AII increased to 229.2 ± 46.65 fmol/ml (p < 0.001) on day 3, prior to the onset of salt appetite on days 4–7. In marked contrast to plasma AII during sodium depletion, CSF AII was unchanged during salt appetite. There was no correlation between plasma and CSF AII during behavioural salt appetite. The CSF AII suggests slight plasma ‘escape’ via circumventricular organs rather than synthesis in the brain, but is not correlated with salt appetite. The effect of sodium depletion on plasma AVP and plasma PRL was to suppress plasma levels consistent with the homeostatic response arising from sodium deficiency. In cattle the perturbations of endogenous neuropeptides evoked during sodium deficit arise from physiological homeostatic responses and are not directly related to salt