CENTRAL OXYTOCIN INHIBITION OF SALT APPETITE IN RATS - EVIDENCE FOR DIFFERENTIAL SENSING OF PLASMA SODIUM AND OSMOLALITY

Sodium chloride ingestion is stimulated during conditions of sodium de ficiency to maintain body fluid and electrolyte balance. Recent studie s have indicated that salt appetite in rats is often inversely related to peripheral and central secretion of the hormone oxytocin (OT). We studied the potential role of central OT on salt and water ingestion b y treating rats intracerebroventricularly with OT conjugated to the A chain of the plant cytotoxin ricin (rAOT) to produce a chronic selecti ve inactivation of brain cells containing OT-receptive elements. The r ats treated with rAOT and control rats treated with the ricin A chain alone were given 5-hr two-bottle (water and 0.5 M NaCl) drinking tests 30 min after they were made hyperosmolar by injections of hypertonic (2 M) mannitol solution, which elevated plasma osmolality but reduced plasma Na+ concentration. In the control rats only water intake was st imulated in response to the induced hyperosmolality, but in the rAOT-t reated rats hypertonic mannitol caused a robust salt appetite as well as thirst. Analogous results were obtained in rats treated with two di fferent OT-receptor antagonists prior to induction of hyperosmolality with mannitol. In contrast to these results, when hyperosmolality was induced by administration of equivalently hypertonic (1 M) NaCl, which elevated both plasma osmolality and plasma Na+ concentration, only wa ter intake but not salt intake was stimulated in both control and OT-r eceptor antagonist-treated rats. When salt appetite was stimulated by the physiological stimulus of polyethylene glycol-induced hypovolemia, hypertonic mannitol similarly inhibited salt ingestion in control ani mals but not in rAOT-treated rats, whereas hypertonic NaCl inhibited s ubsequent salt ingestion in both groups. These results suggest that sa lt appetite is regulated by both Na+- and osmolality-sensing mechanism s in rats. In addition, they indicate that central OT likely mediates a significant component of osmolality-related inhibition of salt appet ite but does not appear to be essential for Na+-related inhibition of this important homeostatic behavior.