Abstract
Sodium appetite is an innate behavior occurring in response to sodium depletion that induces homeostatic responses such as the secretion of the mineralocorticoid hormone aldosterone from the zona glomerulosa of the adrenal cortex and the stimulation of the peptide hormone angiotensin II (ANG II). The synergistic action of these hormones signals to the brain the sodium appetite that represents the increased palatability for salt intake. This narrative review summarizes the main data dealing with the role of mineralocorticoid and ANG II receptors in the central control of sodium appetite. Appropriate keywords and MeSH terms were identified and searched in PubMed. References to original articles and reviews were examined, selected, and discussed. Several brain areas control sodium appetite, including the nucleus of the solitary tract, which contains aldosterone-sensitive HSD2 neurons, and the organum vasculosum lamina terminalis (OVLT) that contains ANG II-sensitive neurons. Furthermore, sodium appetite is under the control of signaling proteins such as mitogen-activated protein kinase (MAPK) and inositol 1,4,5-thriphosphate (IP3). ANG II stimulates salt intake via MAPK, while combined ANG II and aldosterone action induce sodium intake via the IP3 signaling pathway. Finally, aldosterone and ANG II stimulate OVLT neurons and suppress oxytocin secretion inhibiting the neuronal activity of the paraventricular nucleus, thus disinhibiting the OVLT activity to aldosterone and ANG II stimulation.
Highlights
Thirst and sodium appetite represent a pivotal physiological function of all mammals, including humans
It was noted that cFos levels were significantly increased in the organum vasculosum lamina terminalis (OVLT) and suppressed in the paraventricular nucleus (PVN) after a combined administration of angiotensin II (ANG II) and DOCA, suggesting that DOCA stimulates salt intake via attenuation of the responsiveness of PVN OT-ergic neurons to ANG II [48] (Figure 1)
Chronic aldosterone infusion into the 4th ventricle significantly increased the daily intake of sodium chloride (0.3 M). This effect was prevented by the mineralocorticoid receptor (MR) antagonist RU28318, indicating that MRs were required for biological response. These findings suggest that aldosterone, binding to MRs in the central nervous system, activates brain circuits involved in the control of salt appetite [149]
Summary
Thirst and sodium appetite represent a pivotal physiological function of all mammals, including humans. ANG-MAPK signaling stimulates salt intake by modifying neuronal excitability in OVLT, SFO or forebrain integration sites, as NTS and BNT, via regulation of potassium channel subunit [27]. A central infusion of both aldosterone and ANG II leads to a synergistic increase in sodium appetite [38,39] This synergy is selective for salt intake and independent of plasma sodium concentration. XC pretreatment inhibited IP3-induced cFos immunoreactivity significantly in relevant hypothalamic nuclei and CVOs. It was noted that cFos levels were significantly increased in the OVLT and suppressed in the PVN after a combined administration of ANG II and DOCA, suggesting that DOCA stimulates salt intake via attenuation of the responsiveness of PVN OT-ergic neurons to ANG II [48] (Figure 1)
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