Interaction of prolactin, ANPergic, oxytocinergic and adrenal systems in response to extracellular volume expansion in rats

Abstract

The present study evaluated the effect of acute extracellular volume expansion (EVE) induced by intravenous injection of isotonic (0.15 M NaCl) or hypertonic saline (0.3 M NaCl) on prolactin, corticosterone, vasopressin, oxytocin and atrial natriuretic peptide (ANP) secretion. Male Wistar rats were treated with bromocriptine, sulpiride or dexamethasone. After isotonic and hypertonic EVE, the control group showed a significant increase in the plasma concentrations of prolactin, corticosterone, ANP and oxytocin. The increase in ANP and oxytocin levels in response to hypertonic EVE was more pronounced than to isotonic EVE. Bromocriptine and sulpiride treatments did not modify corticosterone, ANP and oxytocin responses to either isotonic or hypertonic EVE. The increases in prolactin and oxytocin, but not ANP, were blocked in dexamethasone pretreated rats. In conclusion, isotonic or hypertonic EVE induced an increase in the plasma concentrations of prolactin, corticosterone, ANP and oxytocin. The increases in ANP and oxytocin were independent of plasma concentrations of prolactin. The increases in prolactin and oxytocin were blocked by the inhibition of the hypothalamo-pituitary-adrenal (HPA) axis by dexamethasone. However, dexamethasone did not alter the increase in ANP secretion induced by isotonic or hypertonic EVE. Therefore, prolactin might participate in regulation of the hydroelectrolytic balance in mammals; however, in the present study, there was no evidence for direct interaction with ANPergic and oxytocinergic systems. In addition, the responses of prolactin and oxytocin induced by isotonic or hypertonic EVE are modulated by the HPA axis.

Central actions of glucocorticoids in the control of body fluid homeostasis: Review

“…On the other hand, rats submitted to hypertonic (1.8% NaCl) BVE presented increased plasma levels of AVP, OT and ANP in order to promote water reabsorption and renal sodium excretion (32)(33)(34).…”

“…In 2004, Durlo et al (33) reported the first evidence for the participation of the HPA axis in hormone secretion induced by BVE in rats. These investigators reported that both hypervolemia and hyperosmolality increased plasma corticosterone concentrations, an event also known to occur in response to other types of stress, such as forced swimming, immobilization and hypoglycemia (35).…”

Changes in prolactin secretion in the short- and long-term after adrenalectomy

“…Although AVP induces prolactin release in vivo (37), we did not observe changes in plasma AVP throughout the time course after ADX surgery (24), suggesting that this peptide might not have a role in prolactin se cretion in this experimental model. We and others have shown an increase in plasma PRL induced by increased water and salt ingestion or after hypertonic EVE infu sion (21,38). However, the increase in PRL and OT levels after isotonic or hypertonic EVE were blocked by glucocorticoid treatment.…”

“…We have previously studied the effect of acute extracellular volume expansion by intravenous injection of isotonic or hypertonic saline on the secre tion of prolactin, corticosterone, vasopressin, oxytocin, and atrial natriuretic peptide. We demonstrated that the increment in prolactin and oxytocin was blocked by the inhibition of the hypothalamuspituitaryadrenal (HPA) axis by dexamethasone (21). Therefore, pro lactin and oxytocin responses induced by isotonic or hypertonic extracellular volume expansion are likely to be modulated by the HPA axis.…”

Novel Aspects of Glucocorticoids Actions on Energy Homeostasis and Hydromineral Balance

“…Accordingly, it has been demonstrated that high doses of dexamethasone can inhibit OT but not AVP secretion in response to hypertonic extracellular volume expansion (Durlo et al, 2004;Ruginsk et al, 2007) and central cholinergic, angiotensinergic and osmotic stimulation (Lauand et al, 2007). These effects were also correlated with immunohistochemical data, showing that the magnocellular neurons of the PVN and SON are inhibited by dexamethasone administration (Ruginsk et al, 2007).…”