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Acute sodium deficit triggers plasticity of the brain angiotensin type 1 receptors
Author(s) -
Charron Geneviève,
Laforest Sylvie,
Gag Caroline,
Drolet Guy,
Mouginot Didier
Publication year - 2002
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.01-0531fje
Subject(s) - subfornical organ , median preoptic nucleus , endocrinology , medicine , angiotensin ii , receptor , hypothalamus , renin–angiotensin system , chemistry , angiotensin receptor , biology , blood pressure
The brain renin‐angiotensin system (bRAS) is involved in the control of hydromineral balance. However, little information is available on the functional regulation of the bRAS as a consequence of sodium deficit in the extracellular fluid compartments. We used a pharmacological model of acute Na + depletion (furosemide injections) to investigate changes of a major component of the bRAS, the hypothalamic angiotensin type 1A (AT 1A ) receptors. Furosemide induced a rapid and long‐lasting expression of the AT 1A mRNA in the subfornical organ, the median preoptic nucleus (MnPO), and the parvocellular division of the paraventricular nucleus (pPVN). Na + depletion increased the number of cells expressing AT 1A mRNA in the pPVN, but not in the MnPO. The enhancement of AT 1A mRNA expression was associated with an increase in AT 1 binding sites in all the regions studied. It is of interest that in the paraventricular nucleus, the majority of the neurons expressing AT 1A mRNA also showed an increase in metabolic activity (Fos‐related antigen immunoreactivity [FRA‐ir]). By contrast, in the MnPO, we observe two distinct cell populations. Our data demonstrated that an acute Na + deficit induced a functional regulation of the hypothalamic AT 1A receptors, indicating that these receptors are subject to plasticity in response to hydromineral perturbations.