Hypertonic NaCl inhibits gastric motility and food intake in rats with lesions in the rostral AV3V region

Abstract

Several diverse treatments that stimulate pituitary secretion of oxytocin (OT) in rats produce a parallel inhibition of gastric motility and food intake. The present experiments demonstrate that injection of hypertonic saline (HS) is another such treatment. Systemic administration of large doses of OT had no effect on gastric motility. Lesions within the region anteroventral to the third ventricle (AV3V region) severely impaired the drinking response to HS without affecting its inhibition of either gastric motility or food intake. These and other results suggest that despite the close association of pituitary secretion of OT with inhibition of both gastric motility and food intake in intact animals after HS administration, these effects may be dissociated by lesions within the AV3V region. Consequently, osmosensitive cells located within the periventricular tissue of the rostral AV3V region, which are critical for the stimulation of thirst and pituitary OT secretion after systemic injection of HS, do not appear to be essential for the parallel inhibition of gastric motility and food intake produced by this treatment in rats.

Organum vasculosum laminae terminalis contributes to increased sympathetic nerve activity induced by central hyperosmolality

“…The OVLT plays a major role in hyperosmolality-stimulated thirst (19,27,28,44,48) and pituitary release of vasopressin (30,44,48) and oxytocin (17,35). To date, however, involvement of OVLT in mediating hyperosmolality-induced increases of SNA has not been directly assessed.…”

Dehydration anorexia is attenuated in oxytocin-deficient mice

“…Before the present study, evidence to support a role for central OT in dehydration anorexia has come primarily from short-term experiments in rats in which osmotic dehydration is induced by systemic administration of hypertonic solutions, and OT signaling is manipulated by central administration of OT receptor agonists and antagonists. Such experiments have demonstrated that OT-containing projections from the PVN to the DVC provide a tonic hypothalamic inhibition of vagally mediated gastric motility and emptying (8,29), that this inhibitory influence is amplified during osmotic dehydration (9), and that OT receptor blockade attenuates both dehydration-induced inhibition of gastric emptying and dehydration anorexia (23).…”

“…Circulating AVP promotes renal retention of water, whereas OT promotes renal excretion of sodium in rats (40). Dehydration also inhibits gastric emptying and food intake (8,30,32,34,42), which together help limit absorption of additional osmoles into the circulation. Finally, dehydration stimulates compensatory drinking of water, when it is available; the subsequent absorption of water into the circulation helps to restore both intracellular and extracellular fluid compartments (31, 34).…”

Ontogeny of hypothalamic-hindbrain feeding control circuits

“…Since hypophagia accompanies states of osmotic dehydration in adult rats, it is significant that this behavioral effect is blunted by central antagonism of OT receptors (Olson, Drutarosky, Stricker, & Verbalis, 1991a). In adult rats, the OT-containing projection from the PVN to the DVC provides a tonic inhibitory influence over vagally mediated gastric motility that is further amplified by plasma hyperosmolality (Flanagan, Blackburn, Verbalis, & Stricker, 1992b;Rogers & Hermann, 1992). Microinjection of OT into the DVC increases the activity of neurons there that receive synaptic input from gastric viscerosensory afferents (McCann & Rogers, 1990), consistent with a role for OT signaling within the DVC to underlie an indirect control of food intake.…”

“…Centrally mediated responses to plasma hyperosmolality in adult rats include compensatory drinking, neurohypophyseal secretion of OT and vasopressin (Stricker & Verbalis, 1986), inhibition of vagally mediated gastric motility and emptying (Flanagan et al, 1989;Flanagan et al, 1992b), and inhibition of food intake (Flanagan, Dohanics, Verbalis, & Stricker, 1992a). The first two responses also occur in neonatal rats (Almli, 1973;Bruno, 1981;Sinding, Robinson, & Seif, 1980), whereas the latter hypophagic response, termed ''dehydration anorexia,'' does not emerge until after the first 2 weeks of postnatal development (Bruno, 1981;Bruno & Hall, 1982;Callahan & Rinaman, 1998).…”