Some factors affecting drinking behavior and their interactions in seawater-acclimated eels, Anguilla japonica

Intravenous administration of eel angiotensin II (eANG II), histamine (HA), serotonin (5-HT), acetylcholine (ACh) or carbachol (CCh), mammalian substa nce P (mSP) and isoproterenol (P-adrenoceptor agonist) enhanced drinking ra te in the seawater eels. The dipsogenic effects of HA and 5-HT seem to be d ue to ANG II synthesis, because these effects were completely blocked by ca ptopril, an inhibitor of angiotensin converting enzyme (ACE). Captopril blo cked eANG I effect, but not eANG II effect, suggesting existence of ACE in seawater eels. 800 mu l Hemorrhage also enhanced water intake, and this eff ect was completely blocked by captopril. Therefore, it is likely that blood withdrawal stimulates renin-angiotensin system (RAS) in seawater eels. Eff ects of ACh, CCh and mSP were not inhibited by captopril, suggesting separa te action of these regulators from ANG II synthesis. Isoproterenol action w as partially inhibited by captopril, suggesting existence of some P-adrenoc eptors other than the RAS. On the other hand, intravenous eel atrial natriu retic peptide (eANP), arginine vasotocin (AVT), human vasoactive intestinal peptide (hVIP), mammalian bradykinin (mBK), eel intestinal pentapeptide (E IPP), cholecystokinin (CCK-8), and phenylephrine (alpha-adrenoceptor agonis t) depressed the drinking rate. In the presence of mBK, HA and 5-HT enhance d water intake similarly as in the absence of mBK. Plasma hyperosmolarity a lso reduced drinking. Although the in vivo system is so complicated and man y regulators are involved in the drinking behavior, a possible regulatory m echanisms are proposed. Compared to mammalian results, eels seem to be a su itable model for anlayzing drinking mechanisms in vertebrates.