Central inhibition of salt appetite by oxytocin in rats

Considerable evidence indicates an important role of hormones in the stimulation 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. Conversely, numerous studies have demonstrated that central oxytocin (OT) provides a stimulus for inhibition of salt appetite. The latter conclusion is supported by the following observations in rats: (a) intracerebroventricular (i.c.v.) injection of OT inhibits salt appetite stimulated by subcutaneous colloid; (b) treatments that inhibit NaCl intake, such as acute hyperosmolality, stimulate pituitary secretion of OT (which is correlated with central release of OT in these studies), whereas treatments that decrease OT secretion, such as systemic injection of deoxycorticosterone and dietary sodium deprivation, potentiate Ang-II-induced NaCl intake; (c) systemic ethanol administration inhibits OT secretion and enhances Ang-II-induced salt appetite; (d) naloxone, which augments stimulated OT secretion, inhibits NaCl appetite induced by colloid treatment, an effect that is abolished by i.c.v. pretreatment with an OT receptor antagonist; and (e) destruction of central neurons bearing OT receptors increases Ang II-induced salt appetite. By mediating the inhibition of NaCl intake in rats, central OT complements the known peripheral effects of OT to facilitate renal sodium excretion.