Blockade of ERK1/2 activation with U0126 or PEP7 reduces sodium appetite and angiotensin II-induced pressor responses in spontaneously hypertensive rats

Andrade-Franzé, G.M.F.; Pereira, Elise de Matos; Yosten, Gina L. C.; Samson, Willis K.; Menani, José Vanderlei; Luca, Laurival A. De; Andrade, C.A.F.

doi:10.1016/j.peptides.2020.170439

Cited by 5 publications

(5 citation statements)

References 31 publications

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“…Knowledge about thirst and sodium appetite's cellular and molecular mechanisms, two physiologically important behaviors, has grown enormously during recent decades 17 , 20 , 42 , 49 . This accumulated evidence opens a new chapter in our understanding of hydroelectrolytic homeostasis.…”

Section: Discussionmentioning

confidence: 99%

“…In this regard, AngII binding to the AT1 stimulates the central AngII system, activating its intracellular pathways implicated in both thirst and induction of SA, specifically involving MAPK signaling in sodium appetite onset 17 – 20 . The rapid pharmacological model of sodium appetite stimulation (FURO + CAP) increased MAPK activity along the CVOs of the lamina terminalis and the PVN/SON hypothalamic areas 18 .…”

Section: Discussionmentioning

confidence: 99%

“…AngII binds the angiotensin II type 1 receptor (AT1) central receptor to induce thirst and sodium appetite, but this hormone recruits different intracellular players to modulate these behaviors 17 – 20 . SFO-AV3V AT1 activation takes the mitogen-activated protein kinase (MAPK) pathway, previously linked to AngII-induced increases in sodium appetite 17 – 26 .…”

Section: Introductionmentioning

confidence: 99%

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Molecular neurobiological markers in the onset of sodium appetite

Porcari

Cambiasso

Mecawi

et al. 2022

Sci Rep

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Sodium appetite is a motivational state involving homeostatic behavior, seeking the ingest of salty substances after sodium loss. There is a temporal dissociation between sodium depletion (SD) and the appearance of sodium appetite. However, the responsible mechanisms for this delay remain poorly elucidated. In the present study, we measured the temporal changes at two and 24 h after SD in the gene expression of key elements within excitatory, inhibitory, and sensory areas implicated in the signaling pathways involved in the onset of sodium appetite. In SD rats, we observed that the expression of critical components within the brain control circuit of sodium appetite, including Angiotensin-type-1 receptor (Agtr1a), Oxytocin-(OXT-NP)-neurophysin-I, and serotonergic-(5HT)-type-2c receptor (Htr2c) were modulated by SD, regardless of time. However, we observed reduced phosphorylation of mitogen-activated protein kinases (MAPK) at the paraventricular nucleus (PVN) and increased oxytocin receptor (Oxtr) mRNA expression at the anteroventral of the third ventricle area (AV3V), at two hours after SD, when sodium appetite is inapparent. At twenty-four hours after SD, when sodium appetite is released, we observed a reduction in the mRNA expression of the transient receptor potential channel 1gene (Trpv1) and Oxtr in the AV3V and the dorsal raphe nucleus, respectively. The results indicate that SD exerts a coordinated timing effect, promoting the appearance of sodium appetite through changes in MAPK activity and lower Trpv1 channel and Oxtr expression that trigger sodium consumption to reestablish the hydroelectrolytic homeostasis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Molecular neurobiological markers in the onset of sodium appetite

Porcari

Cambiasso

Mecawi

et al. 2022

Sci Rep

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“…In addition, the lamina terminalis of this strain expresses more Fos-IR in response to either brain or systemic infusions of ANG II ( Rowland et al, 1995 ; Blume et al, 1997 ). Finally, inhibition of brain AT1R-mediated ERK1/2 activation reduces 0.3 M NaCl intake and the ANG II pressor response in the SHR ( Andrade-Franze et al, 2020 ). Taken together, these findings suggest that the high intake of hypertonic NaCl exhibited by the SHR in response to WD-PR results from hyperactive brain RAS activity, particularly in the lamina terminalis.…”

Section: Sodium Intake and Sodium Palatability In Spontaneously Hyper...mentioning

confidence: 99%

Inhibition of salty taste and sodium appetite by estrogens in spontaneously hypertensive rats

et al. 2023

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“…AT 1R signaling triggers the intracytoplasmic production of the inositol 1,4,5-triphosphate (IP3) and enhances Ca 2+ mobilization [ 43 ]. In addition, extracellular signal-regulated kinase 1 and 2 (ERK 1/2) is activated in the SFO and PVN after central administration of ANG II [ 44 ]. Thus, while the IP3 signaling pathway stimulates thirst by ANG II, the ERK 1/2 signaling is involved in sodium appetite [ 45 ].…”

Section: Introductionmentioning

confidence: 99%

Signal Transduction of Mineralocorticoid and Angiotensin II Receptors in the Central Control of Sodium Appetite: A Narrative Review

Iovino

Messana

Lisco

et al. 2021

IJMS

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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.

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Blockade of ERK1/2 activation with U0126 or PEP7 reduces sodium appetite and angiotensin II-induced pressor responses in spontaneously hypertensive rats

Cited by 5 publications

References 31 publications

Molecular neurobiological markers in the onset of sodium appetite

Molecular neurobiological markers in the onset of sodium appetite

Inhibition of salty taste and sodium appetite by estrogens in spontaneously hypertensive rats

Signal Transduction of Mineralocorticoid and Angiotensin II Receptors in the Central Control of Sodium Appetite: A Narrative Review

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