| Full text | |
| Author(s): |
Monteiro, L. R. N.
[1]
;
Marangon, P. B.
[2]
;
Elias, L. L. K.
[2]
;
Reis, L. C.
[1]
;
Antunes-Rodrigues, J.
[2]
;
Mecawi, A. S.
[1]
Total Authors: 6
|
| Affiliation: | [1] Univ Fed Rural Rio de Janeiro, Inst Biol & Hlth Sci, Dept Physiol Sci, Seropedica, RJ - Brazil
[2] Univ Sao Paulo, Dept Physiol, Fac Med Ribeirao Preto, Ribeirao Preto, SP - Brazil
Total Affiliations: 2
|
| Document type: | Journal article |
| Source: | Journal of Neuroendocrinology; v. 29, n. 9 SEP 2017. |
| Web of Science Citations: | 0 |
| Abstract | |
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. (AU) | |
| FAPESP's process: | 13/09799-1 - Energy balance and body fluid homeostasis control: from cells to the physiological systems |
| Grantee: | José Antunes Rodrigues |
| Support Opportunities: | Research Projects - Thematic Grants |