Intravenous administration of eel angiotensin II (eANG II), histamine (HA), serotonin (5-HT), acetylcholine (ACh) or carbachol (CCh), mammalian substance P (mSP) and isoproterenol (β-adrenoceptor agonist) enhanced drinking rate in the seawater eels. The dipsogenic effects of HA and 5-HT seem to be due to ANG II synthesis, because these effects were completely blocked by captopril, an inhibitor of angiotensin converting enzyme (ACE). Captopril blocked eANG I effect, but not eANG II effect, suggesting existence of ACE in seawater eels. 800 μl Hemorrhage also enhanced water intake, and this effect was completely blocked by captopril. Therefore, it is likely that blood withdrawal stimulates renin-angiotensin system (RAS) in seawater eels. Effects of ACh, CCh and mSP were not inhibited by captopril, suggesting separate action of these regulators from ANG II synthesis. Isoproterenol action was partially inhibited by captopril, suggesting existence of some β-adrenoceptors other than the RAS. On the other hand, intravenous eel atrial natriuretic peptide (eANP), arginine vasotocin (AVT), human vasoactive intestinal peptide (hVIP), mammalian bradykinin (mBK), eel intestinal pentapeptide (EIPP), cholecystokinin (CCK-8), and phenylephrine (α-adrenoceptor agonist) depressed the drinking rate. In the presence of mBK, HA and 5-HT enhanced water intake similarly as in the absence of mBK. Plasma hyperosmolarity also reduced drinking. Although the in vivo system is so complicated and many regulators are involved in the drinking behavior, a possible regulatory mechanisms are proposed. Compared to mammalian results, eels seem to be a suitable model for anlayzing drinking mechanisms in vertebrates.