Osmoreceptor mechanism for oxytocin release in the rat.

Abstract

In order to determine whether oxytocin release is controlled by an osmoreceptor mechanism identical with that for vasopressin release, the plasma oxytocin concentration and plasma osmolality were measured during intraatrial infusion and after intraventricular injection of various osmotic solutions in unanesthetized rats. Intraatrial infusion of 0.6 M NaCI Locke solution (LS.) or 1.2 M mannitol L.S. elevated plasma oxytocin significantly, while 1.2 M urea L.S. caused only a small increase and isotonic L.S. did not change in plasma oxytocin. All hypertonic solutions produced significant and similar increases in the plasma osmolality. Plasma oxytocin was positively correlated with plasma osmolality in the animals infused with hypertonic NaCI or mannitol but not in the animals infused with hypertonic urea. The injection of 2 tl of 0.6 M NaCI artificial cerebrospinal fluid (CSF) or 1.2 M mannitol CSF into the third ventricle caused a significant increase in plasma oxytocin immediately (5 min after injection) without changing plasma osmolality, while the intraventricular injection of 1.2 M urea CSF or isotonic CSF produced no significant change in plasma oxytocin. These results indicate that oxytocin release is controlled by osmoreceptors rather than Na receptors, that the adequate stimulus for the osmoreceptors is one which produces cellular dehydration and that the osmoreceptors are located in the brain region which is accessible to osmotic agents from both the outside and inside of the bloodbrain barrier. Since the organum vasculosum of the lamina terminalis (OVLT) lacks a blood-brain barrier and is known to be involved in osmotic control of vasopressin release, a lesion was made in the anteroventral region of the third ventricle which encompasses the OVLT and the effect of hypertonic NaCI infusion on oxytocin release was examined. No significant increase in plasma oxytocin was observed after intraatrial infusion of 0.6 M NaCI L.S. in the lesioned rats. All of these findings lead to the conclusion that oxytocin release is under the control of osomoreceptors identical to those for vasopressin release.

Oxytocinergic and serotonergic systems involvement in sodium intake regulation: satiety or hypertonicity markers?

“…Lesion studies have shown the participation of important brain nuclei in the oxytocin and vasopressin regulation. For example, the destruction of osmoreceptors in the OVLT and AP eliminates secretion of AVP and OT induced by the sodium loads administered (20,35). SON and PVN receive afferent fibers from the brain stem, such as NTS, LPBN, and raphé nucleus (5-HT afferent), which carry visceral and cardiovascular information (1,18,41).…”

Electrical Activities of Neurones in the Dorsomedial Hypothalamic Nucleus Projecting to the Supraoptic Nucleus During Milk-ejection Reflex in the Rat

“…56: [336][337][338][339][340] 2010) xytocin (OT) is synthesized in the cell body of the OT cell in the hypothalamic paraventricular (PVN) and supraoptic nuclei (SON) and released into blood circulation from axon terminals in the neurohypophysis. Various kinds of physiological stimuli such as parturition, lactation, osmotic stimulus and stress are known to stimulate OT secretion [1][2][3][4]. In lactating rats, OT is released intermittently as a result of periodic and synchronized activation of OT cells distributed in both sides of the hypothalamus, whereas pups suck nipples continuously [5].…”

Synaptic control of rat supraoptic neurones during osmotic stimulation of the organum vasculosum lamina terminalis in vitro.

“…Recent studies have indicated that the anteroventral region of the third ventricle may represent an important source of afferents for the osmotic regulation of the hypothalamo-neurohypophysial system. In particular, lesions encompassing the organum vasculosum lamina terminalis (OVLT) have been found to attenuate the secretion of both oxytocin (Russell, Hatton & Robinson, 1984;Blackburn, Leng & Russell, 1986;Negoro, Higuchi, Tadokoro & Honda, 1988;Leng, Blackburn, Dyball & Russell, 1989) and vasopressin (Russell et al 1984;Leng et al 1989), and to attenuate the electrical response of MNCs following rises in systemic osmolality (Chaudhry, Dyball, Honda & Wright, 1989;Leng et al 1989). These findings have been supported by anatomical (e.g.…”