Estradiol and angiotensin II crosstalk in hydromineral balance: Role of the ERK1/2 and JNK signaling pathways

Almeida-Pereira, Gislaine; Coletti, Ricardo; Mecawi, André Souza; Reis, L. C.; Elias, Lucila Leico Kagohara

doi:10.1016/j.neuroscience.2016.02.067

Cited by 18 publications

(39 citation statements)

References 60 publications

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“…Upon activation, ERK has several targets to possibly influence a wide range of cellular processes, which include the modulation of gene expression via interaction with transcription factors that are then translocated to the cell nucleus; alteration of synaptic plasticity, modulation of dendritic branching and the formation of synaptic contacts; and induction of the phosphorylation of potassium channels leading to down‐regulation and decreased membrane permeability to K + , which increases cellular excitability A recent study showed that phosphorylation of ERK1/2 and c‐Jun N‐terminal kinase in the laminae terminalis is involved in the water and sodium intake in female rats. Interestingly, the present study also found that Ang II‐induced AVP secretion but not oxytocin secretion required ERK1/2 signalling, suggesting that the recruitment of this signalling pathway may vary among the different hypothalamic nuclei …”

Section: Discussionsupporting

confidence: 58%

“…Interestingly, the present study also found that Ang II-induced AVP secretion but not oxytocin secretion required ERK1/2 signalling, suggesting that the recruitment of this signalling pathway may vary among the different hypothalamic nuclei. 32 Thus, based on the present subchronic protocol for inducing sodium appetite and assess the effects of ERK on cellular activity, our data suggest the involvement of Ang II in the plastic changes that lead to the induction of sodium appetite after low-sodium diet consumption.…”

Section: Discussionmentioning

confidence: 56%

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Sodium appetite elicited by low‐sodium diet is dependent on p44/42 mitogen‐activated protein kinase (extracellular signal‐regulated kinase 1/2) activation in the brain

Monteiro

Marangon

Elias

et al. 2017

J Neuroendocrinology

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Sodium appetite is regulated by several signalling molecules, among which angiotensin II (Ang II) serves as a key driver of robust salt intake by binding to Ang II type 1 receptors (AT1R) in several regions in the brain. The activation of these receptors recruits the mitogen-activated protein kinase (MAPK) pathway, which has previously been linked to Ang II-induced increases in sodium appetite. Thus, we addressed the involvement of MAPK signalling in the induction of sodium appetite after 4 days of low-sodium diet consumption. An increase in extracellular signal-regulated kinase (ERK) phosphorylation in the laminae terminalis and mediobasal hypothalamus was observed after low-sodium diet consumption. This response was reduced by i.c.v. microinjection of an AT1R antagonist into the laminae terminalis but not the hypothalamus. This result indicates that low-sodium diet consumption activates the MAPK pathway via Ang II/AT1R signalling on the laminae terminalis. On the other hand, activation of the MAPK pathway in the mediobasal hypothalamus after low-sodium diet consumption appears to involve another extracellular mediator. We also evaluated whether a low-sodium diet could increase the sensitivity for Ang II in the brain and activate the MAPK pathway. However, i.c.v. injection of Ang II increased ERK phosphorylation on the laminae terminalis and mediobasal hypothalamus; this increase achieved a response magnitude similar to those observed in both the normal and low-sodium diet groups. These data indicate that low-sodium diet consumption for 4 days is insufficient to change the ERK phosphorylation response to Ang II in the brain. To investigate whether the MAPK pathway is involved in sodium appetite after low-sodium diet consumption, we performed i.c.v. microinjections of a MAPK pathway inhibitor (PD98059). PD98059 inhibited both saline and water intake after low-sodium diet consumption. Thus, the MAPK pathway is involved in promoting the sodium appetite after low-sodium diet consumption.

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Section: Discussionsupporting

confidence: 58%

Section: Discussionmentioning

confidence: 56%

Sodium appetite elicited by low‐sodium diet is dependent on p44/42 mitogen‐activated protein kinase (extracellular signal‐regulated kinase 1/2) activation in the brain

Monteiro

Marangon

Elias

et al. 2017

J Neuroendocrinology

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“…Estradiol, through the estrogen receptor, is reported to reduce ANG II-induced sodium intake and water intake within the lamina terminalis through inhibition of ERK1/2 and JNK, respectively. In addition, estradiol prevents arginine vasopressin (AVP) secretion in the hypothalamus through MKP1-mediated ERK1/2 dephosphorylation (26). With the use of double transgenic mice to cause ANG II-dependent hypertension, it has been demonstrated that AT 1 R mediates brain ACE2 inhibition (1167).…”

Section: Sympathoexcitatory Actionmentioning

confidence: 99%

Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology

Forrester

Booz

Sigmund

et al. 2018

Physiological Reviews

816

780

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The renin-angiotensin-aldosterone system plays crucial roles in cardiovascular physiology and pathophysiology. However, many of the signaling mechanisms have been unclear. The angiotensin II (ANG II) type 1 receptor (ATR) is believed to mediate most functions of ANG II in the system. ATR utilizes various signal transduction cascades causing hypertension, cardiovascular remodeling, and end organ damage. Moreover, functional cross-talk between ATR signaling pathways and other signaling pathways have been recognized. Accumulating evidence reveals the complexity of ANG II signal transduction in pathophysiology of the vasculature, heart, kidney, and brain, as well as several pathophysiological features, including inflammation, metabolic dysfunction, and aging. In this review, we provide a comprehensive update of the ANG II receptor signaling events and their functional significances for potential translation into therapeutic strategies. ATR remains central to the system in mediating physiological and pathophysiological functions of ANG II, and participation of specific signaling pathways becomes much clearer. There are still certain limitations and many controversies, and several noteworthy new concepts require further support. However, it is expected that rigorous translational research of the ANG II signaling pathways including those in large animals and humans will contribute to establishing effective new therapies against various diseases.

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“…The renin-angiotensin system (RAS) plays an essential role in the maintenance of hydromineral homeostasis by eliciting sodium and water intake and by inducing sodium urinary retention through aldosterone release and hemodynamic effects via angiotensin II a key component of the RAS (Hollenberg 1984, Fitzsimons 1998. The octapeptide hormone angiotensin II (ANGII) also induces vasopressin (AVP) and oxytocin (OT) secretion when injected into the brain (Antunes-Rodrigues et al 2004, Almeida-Pereira et al 2016. OT and AVP are synthesized by magnocellular neurosecretory neurons of the paraventricular (PVN) and the supraoptic (SON) hypothalamic nuclei and are released into the circulation from the neurohypophysis.…”

Section: Introductionmentioning

confidence: 99%

17β-Estradiol attenuates p38MAPK activity but not PKCα induced by angiotensin II in the brain

Almeida-Pereira

Vilhena‐Franco

Coletti

et al. 2019

Journal of Endocrinology

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17β-Estradiol (E2) has been shown to modulate the renin–angiotensin system in hydromineral and blood pressure homeostasis mainly by attenuating angiotensin II (ANGII) actions. However, the cellular mechanisms of the interaction between E2 and angiotensin II (ANGII) and its physiological role are largely unknown. The present experiments were performed to better understand the interaction between ANGII and E2 in body fluid control in female ovariectomized (OVX) rats. The present results are the first to demonstrate that PKC/p38 MAPK signaling is involved in ANGII-induced water and sodium intake and oxytocin (OT) secretion in OVX rats. In addition, previous data from our group revealed that the ANGII-induced vasopressin (AVP) secretion requires ERK1/2 signaling. Therefore, taken together, the present observations support a novel concept that distinct intracellular ANGII signaling gives rise to distinct neurohypophyseal hormone release. Furthermore, the results show that E2 attenuates p38 MAPK phosphorylation in response to ANGII but not PKC activity in the hypothalamus and the lamina terminalis, suggesting that E2 modulates ANGII effects through the attenuation of the MAPK pathway. In conclusion, this work contributes to the further understanding of the interaction between E2 and ANGII signaling in hydromineral homeostasis, as well as it contributes to further elucidate the physiological relevance of PKC/p38 MAPK signaling on the fluid intake and neurohypophyseal release induced by ANGII.

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Estradiol and angiotensin II crosstalk in hydromineral balance: Role of the ERK1/2 and JNK signaling pathways

Cited by 18 publications

References 60 publications

Sodium appetite elicited by low‐sodium diet is dependent on p44/42 mitogen‐activated protein kinase (extracellular signal‐regulated kinase 1/2) activation in the brain

Sodium appetite elicited by low‐sodium diet is dependent on p44/42 mitogen‐activated protein kinase (extracellular signal‐regulated kinase 1/2) activation in the brain

Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology

17β-Estradiol attenuates p38MAPK activity but not PKCα induced by angiotensin II in the brain

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