Oxytocin in the Central Amygdaloid Nucleus Modulates the Neuroendocrine Responses Induced by Hypertonic Volume Expansion in the Rat

Abstract

The present study investigated the involvement of the oxytocinergic neurones that project into the central amygdala (CeA) in the control of electrolyte excretion and hormone secretion in unanaesthetised rats subjected to acute hypertonic blood volume expansion (BVE; 0.3 M NaCl, 2 ml/100 g of body weight over 1 min). Oxytocin and vasopressin mRNA expression in the paraventricular (Pa) and supraoptic nucleus (SON) of the hypothalamus were also determined using the real time-polymerase chain reaction and in situ hybridisation. Male Wistar rats with unilaterally implanted stainless steel cannulas in the CeA were used. Oxytocin (1 μg/0.2 μl), vasotocin, an oxytocin antagonist (1 μg/0.2 μl) or vehicle was injected into the CeA 20 min before the BVE. In rats treated with vehicle in the CeA, hypertonic BVE increased urinary volume, sodium excretion, plasma oxytocin (OT), vasopressin (AVP) and atrial natriuretic peptide (ANP) levels and also increased the expression of OT and AVP mRNA in the Pa and SON. In rats pre-treated with OT in the CeA, previously to the hypertonic BVE, there were further significant increases in plasma AVP, OT and ANP levels, urinary sodium and urine output, as well as in gene expression (AVP and OT mRNA) in the Pa and SON compared to BVE alone. Vasotocin reduced sodium, urine output and ANP levels, although no changes were observed in plasma AVP and OT levels or in the expression of the AVP and OT genes in both hypothalamic nuclei. The results of the present study suggest that oxytocin in the CeA exerts a facilitatory role in the maintenance of hydroelectrolyte balance in response to changes in extracellular volume and osmolality.

Cardiovascular Action of Oxytocin

“…It has been observed that isotonic volume expansion by intra-atrial injection of isotonic saline induced a rapid increase in plasma oxytocin and ANP concentrations and a concomitant decrease in plasma vasopressin concentration, and that oxytocin (I.P.) injected caused a significant increase in urinary osmolality, natriuresis and plasma ANP level [28]. Because it is known that loss of blood volume stimulates release of vasopressin from hypothalamus-pituitary, which decreases release of ANP from atria.…”

“…Because it is known that loss of blood volume stimulates release of vasopressin from hypothalamus-pituitary, which decreases release of ANP from atria. It has been hypothesized that volumeexpansion stimulates release of neuropeptide oxytocin from hypothalamus-pituitary into blood, which circulated to the atria to stimulate ANP release and promote natriuresis [28]. Therefore, a dedicated balance between two neuropeptides released from hypothalamus-pituitary may be critical for maintenance of body volume homeostasis and blood pressure regulation.…”