CENTRAL INHIBITION OF SALT APPETITE BY OXYTOCIN IN RATS

Considerable evidence indicates an important role of hormones in the s timulation of fluid consumption. For example, angiotensin II (Ang II), together with afferent neural input from cardiovascular baroreceptors , is well known to stimulate thirst and NaCl intake in rats. Conversel y, numerous studies have demonstrated that central oxytocin (OT) provi des a stimulus for inhibition of salt appetite. The latter conclusion is supported by the following observations in rats: (a) intracerebrove ntricular (i.c.v.) injection of OT inhibits salt appetite stimulated b y subcutaneous colloid; (b) treatments that inhibit NaCl intake, such as acute hyperosmolality, stimulate pituitary secretion of OT (which i s correlated with central release of OT in these studies), whereas tre atments that decrease OT secretion, such as systemic injection of deox ycorticosterone and dietary sodium deprivation, potentiate Ang-II-indu ced NaCl intake; (c) systemic ethanol administration inhibits OT secre tion and enhances Ang-II-induced salt appetite; (d) naloxone, which au gments stimulated OT secretion, inhibits NaCl appetite induced by coll oid treatment, an effect that is abolished by i.c.v. pretreatment with an OT receptor antagonist; and (e) destruction of central neurons bea ring OT receptors increases Ang II-induced salt appetite. By mediating the inhibition of NaCl intake in rats, central OT complements the kno wn peripheral effects of OT to facilitate renal sodium excretion.