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 presystemic 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 (~1.7 ml/min) and emptied ingested fluid from the stomach at a slower but maximally fast rate (~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 (~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 (~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 and integrate these two variables, and thereby modulate the rates of Na + intake and gastric emptying. Keywords adrenalectomy; DOCA; gastric distension; gastric emptying; salt appetite Adrenalectomized (adrex) rats adaptively compensate for the uncontrolled loss of Na + in urine due to the absence of aldosterone by consuming sufficient NaCl solution to maintain Na + balance (12). When adrex rats are deprived of dietary NaCl and become Na + -deficient, they drink a large bout of saline when it becomes available again but stop before their physiological need for Na + has been fully satisfied (9). The issues under investigation in the present experiments are the bases for the termination of that initial drinking bout and the fate of the ingested fluid.A pronounced salt appetite also is seen in rats given daily injections of the synthetic mineralocorticoid, deoxycorticosterone acetate (DOCA) (11), even though those animals have Address for editorial correspondence: Dr. Edward M. Stricker, Department of Neuroscience, 360 Langley Hall, University of Pittsburgh, Pittsburgh, PA 15260, Phone: 412/624-4569, Fax: 412/624-9198, e-mail: stricker@bns.pitt.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors m...