Previous studies have reported that rats drink more saline after area postrema has been removed. The results presented here indicate that prolonged administration of angiotensin II into area postrema of unrestrained rats at 4 pmol/h also caused them to drink more saline. They drank more when angiotensin was released in the anterolateral part of the organ than when it was released anteromedially. Diurnal variation of drinking was not disordered. Dose-response curves showed that rats lacking area postrema drank more saline in response to systemic angiotensin than sham operated animals. The very large 'spontaneous' consumption of saline by rats lacking area postrema was not diminished by saralasin, an angiotensin antagonist. It is concluded that area postrema is a site where systemic angiotensin can act to promote sodium consumption: and that although removing area postrema increases the sensitivity of the drinking response to systemic angiotensin, this enhanced sensitivity is not the cause of the increased sodium consumption.