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

Autor: Carol F. Elias, José Antunes-Rodrigues, Lisandra Oliveira Margatho, L. L. K. Elias
Rok vydání: 2013
Předmět:
Zdroj: Repositório Institucional da USP (Biblioteca Digital da Produção Intelectual)
Universidade de São Paulo (USP)
instacron:USP
ISSN: 0953-8194
Popis: The present study investigated the involvement of the oxytocinergic neurones that project intothe central amygdala (CeA) in the control of electrolyte excretion and hormone secretion in un-anaesthetised 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 theparaventricular (Pa) and supraoptic nucleus (SON) of the hypothalamus were also determinedusing the real time-polymerase chain reaction and in situ hybridisation. Male Wistar rats withunilaterally implanted stainless steel cannulas in the CeA were used. Oxytocin (1 lg/0.2 ll),vasotocin, an oxytocin antagonist (1 lg/0.2 ll) or vehicle was injected into the CeA 20 minbefore 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 significantincreases in plasma AVP, OT and ANP levels, urinary sodium and urine output, as well as in geneexpression (AVP and OT mRNA) in the Pa and SON compared to BVE alone. Vasotocin reducedsodium, urine output and ANP levels, although no changes were observed in plasma AVP andOT levels or in the expression of the AVP and OT genes in both hypothalamic nuclei. The resultsof the present study suggest that oxytocin in the CeA exerts a facilitatory role in the mainte-nance of hydroelectrolyte balance in response to changes in extracellular volume and osmolality.Key words: central amygdaloid nucleus, blood volume expansion, oxytocin, vasopressin, atrialnatriuretic peptidedoi: 10.1111/jne.12021It is well established that blood volume expansion (BVE) induces,via reflex mechanisms, several regulatory responses, including theinhibition of sympathetic outflow to the kidney, heart and bloodvessels; the reduction of renin and vasopressin secretion; and anincrease in the release of atrial natriuretic peptide (ANP) and oxyto-cin (OT) that leads to diuresis and natriuresis (1,2).The central amygdaloid nucleus (CeA) was reported to be animportant constituent of the central pathways that regulate cardio-vascular function and the hormonal and behavioural responses thatminimise and correct sodium deficits (3). Lesions and chemicalstimulation of the amygdaloid complex inhibit sodium chlorideintake (4). In addition, Galaverna et al. (5) showed that lesions ofthe CeA impair both need-free and need-induced NaCl intake. Ratswith lesions of the CeA also fail to ingest 0.5 M NaCl in responseto activation of angiotensin in the brain, or to systemic mineralo-corticoids that produce a vigorous NaCl appetite in control rats.Andrade-Franze et al. (6) postulated that the facilitatory mecha-nisms present in the CeA are essential for the increase in waterand hypertonic NaCl intake produced by blockade of the inhibitorymechanisms of the lateral parabrachial nucleus (LPBN) in furose-mide + low dose of captopril treated rats. In addition, it was shownthat the integrity of the CeA is crucial for the increase in fluidintake produced by serotonergic blockade or by a
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