Previous studies have suggested that angiotensin (ANG) synthesis, receptor activation, or both, in the median preoptic nucleus (MnPO) are responsible for initiating ANG-related salt appetite in normotensive rats. The present study was designed to test whether treatment with saralasin (Sar), an ANG II antagonist, in the MnPO area causes changes in saline (0.3 M NaCl solution) and water intakes in the spontaneously hypertensive rat (SHR), which is known to show greater salt appetite compared to normotensive Wistar-Kyoto (WKY) rats. Treatment with Sar in the MnPO area produced significantly attenuated saline intake, but had no effect on water intake. The results may support the importance of the ANG system in the MnPO area for salt appetite, and suggest that a disorder in the system may cause abnormal salt intake in SHR.