Adrenalectomized (adrex) rats adaptively increase NaCl intake to compensate for the uncontrolled loss of Na(+) in urine due to the absence of aldosterone. After a period of NaCl deprivation, they ingest saline avidly but stop drinking before hyponatremia is repaired. The present experiments determined whether pre-systemic signals inhibit further NaCl intake, and whether gastric emptying of Na(+) is modulated according to the concentration of ingested NaCl solution. After overnight deprivation, adrex rats consumed 0.05 M and 0.15 M NaCl at a maximally fast rate ( approximately 1.7 ml/min) and emptied ingested fluid from the stomach at a slower but maximally fast rate ( approximately 1.1 ml/min). When 0.30 M NaCl was consumed instead, fluid intake still was maximally fast but gastric emptying slowed in proportion to concentration so that the emptying of Na(+) was comparable to that observed when 0.15 M NaCl was ingested ( approximately 0.13 meq/min). When 0.50 M NaCl was consumed, intake slowed proportionately so that Na(+) consumption was comparable to that observed when 0.30 M NaCl was ingested ( approximately 0.5 meq/min). NaCl intake appeared to be inhibited both by the concentration of saline emptied from the stomach and by the volume of ingested fluid in the stomach and small intestine. Gastric emptying also slowed proportionately when 0.50 M NaCl was consumed, as if the rats were regulating the delivery of Na(+) to the small intestine. These results suggest that adrex rats can detect the volume and concentration of ingested NaCl solution presystematically and integrate these two variables, and thereby modulate the rates of Na(+) intake and gastric emptying.