Acute sodium deficit induces functional upregulation and plasticity of hypothalamic AT(1A) receptors, highlighting the brain renin-angiotensin system's role in hydromineral balance.
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Extends rodent evidence for brain AT1 receptor plasticity in sodium balance; leaves open translation to human cardiovascular or HF research.
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.
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Charron et al. (2002) studied this question.
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