Rapid stimulation of sodium intake combining aldosterone into the 4th ventricle and the blockade of the lateral parabrachial nucleus

Abstract

Chronic infusion of aldosterone into the 4th ventricle (4th V) induces robust daily sodium intake, whereas acute injection of aldosterone into the 4th V produces no sodium intake. The inhibitory mechanism of the lateral parabrachial nucleus (LPBN) restrains sodium intake induced by different natriorexigenic stimuli and might affect the acute response to aldosterone into the 4th V. In the present study, 1.8% NaCl and water intake was tested in rats treated with acute injections of aldosterone into the 4th V combined with the blockade of the inhibitory mechanisms with injections of moxonidine (α adrenergic/imidazoline agonist) or methysergide (a serotonergic antagonist) into the LPBN. Male Holtzman rats with stainless steel cannulas implanted in the 4th V and bilaterally in the LPBN were used. Aldosterone (250 or 500ng) into the 4th V combined with vehicle into the LPBN induced no 1.8% NaClintake compared to control (1.5±1.1 and 1.1±0.4, respectively, vs. vehicle into 4th V: 1.0±0.5ml/2h). However, aldosterone (250 or 500ng) into the 4th V combined with moxonidine (0.5nmol) into the LPBN induced strong ingestion of 1.8% NaCl (12.7±4.6 and 17.6±3.7ml/2h, respectively). Aldosterone (250ng) into the 4th V combined with methysergide (4μg) into the LPBN also induced 1.8% NaCl intake (17.6±5.4ml/2h). These data suggest that the inhibitory mechanisms of the LPBN counteract the facilitation of sodium intake produced by aldosterone injected into the 4th, restraining sodium intake in this condition.

The osmoresponsiveness of oxytocin and vasopressin neurones: Mechanisms, allostasis and evolution

“…Electrolyte homeostasis necessarily involves the regulation of both sodium excretion and sodium intake. Dietary sodium deprivation elicits a strong salt appetite in rats, 86 as does bilateral adrenalectomy, 87,88 aldosterone via its actions on the brain, 89,90 and hypovolaemic stimuli. [91][92][93] The AV3V region is strongly implicated in salt appetite, in part via central angiotensin II pathways from the subfornical organ.…”

The role of central amygdaloid nucleus in regulating the nongenomic effect of aldosterone on sodium intake in the nucleus tractus solitary

“…As the critical component of the amygdaloid nucleus, the CeA receives ascending fiber projections of many nuclei in the brainstem, while it emits fiber projections to the dorsal nucleus of the vagus nerve, solitary nucleus, periaqueductal gray matter, and reticular nuclei of the pons. Recent studies have demonstrated that a close fiber link exists between the CeA and a number of regions of the brain associated with sodium intake regulation, such as signals from the HSD2 neuron (Geerling et al., 2006 ; Resch et al., 2017 ) in the solitary nucleus, relayed by the parabrachial nucleus, projected upward to the lateral CeA, and then projected directly by the medial CeA to the HSD2 neuron, which may be an important neural loop where the CeA participates in the regulation of sodium intake (Gasparini et al., 2017 ). In addition, the CeA has a fibrous connection with the nucleus of the reward system and emits fiber projections to neuroendocrine nuclei, such as the chamber nucleus.…”