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

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Abstract
Sodium appetite is regulated by several signalling molecules, among which angiotensinII(Ang II) serves as a key driver of robust salt intake by binding toAng IItype 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 toAng II‐induced increases in sodium appetite. Thus, we addressed the involvement ofMAPKsignalling 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 anAT1R antagonist into the laminae terminalis but not the hypothalamus. This result indicates that low‐sodium diet consumption activates theMAPKpathway viaAng II/AT1R signalling on the laminae terminalis. On the other hand, activation of theMAPKpathway 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 forAng IIin the brain and activate theMAPKpathway. However, i.c.v. injection ofAng IIincreasedERKphosphorylation 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 theERKphosphorylation response toAng IIin the brain. To investigate whether theMAPKpathway is involved in sodium appetite after low‐sodium diet consumption, we performed i.c.v. microinjections of aMAPKpathway inhibitor (PD98059).PD98059 inhibited both saline and water intake after low‐sodium diet consumption. Thus, theMAPKpathway is involved in promoting the sodium appetite after low‐sodium diet consumption.
Funding Information
  • Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro (E-26/203.190/2016)
  • Fundação de Amparo à Pesquisa do Estado de São Paulo (2013/09799-1)
  • Conselho Nacional de Desenvolvimento Científico e Tecnológico (462190/2014-5)

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