Chronic estrogen and 5‐HT1A agonist treatment reduce sodium appetite in ovariectomized rats

Abstract

We have shown that ovarariectomized (OVX) rats exhibited higher salt intake compared to estrogen‐replaced rats (OVX+E2) particularly in models of induction of sodium appetite dependent on angiotensin II and low sodium plasma levels. This result was ascribed to enhanced AT1 receptors activity. In male rats we reported that repeated 5‐HT1A agonist administration reduced sodium appetite response related to somatodendritic 5‐HT1A autoreceptor desensitization. Therefore, we investigate the effect of systemic acute and chronic 8‐OH‐DPAT administration on the sodium appetite in normally hydrated or sodium‐depleted Wistar rats (furosemide, 20mg/kg, sc, 24h before experiment) in OVX+oil and OVX estrogen replaced (OVX+E2, estradiol cypionate, 10μg/animal) rats. Acute 8‐OH‐DPAT (250μg/kg, ip, during 7 days) induced an increase of 0.3M NaCl intake. OVX+E2 rats were not responsive to 5‐HT1A agonist in basal condition. Chronic administration of 8‐OH‐DPAT reduced the saline intake compared to OVX+vehicle, control group (2.3±0.17ml/100g vs 4.2±0.2ml/100g, at 120 min after fluids presentation) in sodium‐depleted rats. E2 replacement strengthened the antinatriorexigenic response of OVX+8‐OH‐DPAT treated rats (1.7±0.1ml/100g vs 4.2ml/100g, at 120 min after fluids presentation). Results suggest that chronic administration of 5‐HT1A agonist associated with E2 replacement therapy differentially trigger mechanisms for neural signaling to sodium satiety, possibly through recruitment of serotonergic pathways in the dorsal raphe nucleus.Support: FAPERJ & CNPq