Eels seem to be a suitable model system for analysing regulatory mechanisms of drinking behavior in vertebrates, since most dipsogens and antidipsogens in mammals influence the drinking rate in the seawater eels similarly. The drinking behavior in fishes consists of swallowing alone, since they live in water and water is constantly held in the mouth for respiration. Therefore, contraction of the upper esophageal sphincter (UES) muscle limits the drinking rate in fishes. The UES of the eel was innervated by the glossopharyngeal-vagal motor complex (GVC) in the medulla oblongata (MO). The GVC neurons were immunoreactive to an antibody raised against choline acetyltransferase (ChAT), an acetylcholine (ACh) synthesizing enzyme, indicating that the eel UES muscle is controlled cholinergically by the GVC. The neuronal activity of the GVC was inhibited by adrenaline or dopamine, suggesting catecholaminergic innervation to the GVC. The AP and the commissural nucleus of Cajal (NCC) in the MO projected to the GVC and were immunoreactive to an antibody raised against tyrosine hydroxylase (TH), rate limiting enzyme to produce catecholamines from tyrosine. Therefore, it is likely that activation in the AP or the NCC may inhibit the GVC and thus relaxes the UES muscle, which allows for water to enter into the esophagus. During passing through the esophagus, the imbibed sea water (SW) was desalted to approximately 1/2 SW, which was further diluted in the stomach and arrived at the intestine as approximately 1/3 SW, almost isotonic to the plasma. Finally, from the diluted SW, the eel intestine absorbed water following the Na(+)-K(+)-2Cl(-) cotransport (NKCC2) system. The NaCl and water absorption across the intestine was regulated by various factors, especially by peptides such as atrial natriuretic peptide (ANP) and somatostatin (SS-25 II). During desalination in the esophagus, however, excess salt enters into the blood circulation, which is liable to raise the plasma osmolarity. However, the eel heart was constricted powerfully by the hyperosmolarity, suggesting that the hyperosmolarity enhances the stroke volume to the gill, where excess salt was extruded powerfully via Na(+)-K(+)-2Cl(-) cotransport (NKCC1) system.