RGD Reference Report - Distinct mechanisms underlie the regulation of body fluid balance by neurokinin B and angiotensin II in the rat brain. - Rat Genome Database

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Distinct mechanisms underlie the regulation of body fluid balance by neurokinin B and angiotensin II in the rat brain.

Authors: Asami, R  Ono, K  Nakanishi, O  Inenaga, K 
Citation: Asami R, etal., Brain Res. 2011 Apr 6;1383:179-86. Epub 2011 Jan 28.
RGD ID: 5129187
Pubmed: PMID:21281609   (View Abstract at PubMed)
DOI: DOI:10.1016/j.brainres.2011.01.072   (Journal Full-text)

Although central injections of either neurokinin B (NKB) or angiotensin II (ANGII) induce a pressor response, they show different involvements in fluid intake behaviors. The aim of the present study was to elucidate the mechanisms by which these two peptides regulate body fluid balance in rats. We demonstrate that intracerebroventricular injections of NKB (1nmol) and ANGII (0.1nmol) both induce pressor responses. However, only ANGII induced significant water intake and increased sodium preference. Co-injection of NKB suppressed the ANGII-induced sodium preference but did not affect the ANGII-induced water intake. Immunohistochemistry for c-Fos, a marker of neuronal activation, revealed that both NKB and ANGII increased neuronal activation in the circumventricular organs and the hypothalamic paraventricular and supraoptic nuclei. In contrast, only ANGII significantly increased c-Fos immunoreactivity in the paraventricular thalamic nucleus, the central amygdala (CeA) and the ventrolateral bed nucleus of the stria terminalis (BSTvl). Co-injection of NKB suppressed the ANGII-induced c-Fos expression in the CeA and BSTvl. These results suggest that centrally injected NKB and ANGII lead to common cardiovascular responses by neuronal pathways through the circumventricular organs and hypothalamus but that they regulate fluid intake behaviors through different pathways. It is likely that the opposing effects of these two peptides on sodium preference can be explained by their differential actions in the CeA and BSTvl, both of which are inhibited by NKB and activated by ANGII.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
angiotensin-mediated drinking behavior  IDA 5129187 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Agt  (angiotensinogen)


Additional Information