Dietary sodium deprivation evokes activation of brain regional neurons and down-regulation of angiotensin II type 1 receptor and angiotensin-convertion enzyme mRNA expression

Lü, Bo; Yang, Xiaojun; Chen, K.; Yang, Deye; Yan, Jiaqi

doi:10.1016/j.neuroscience.2009.08.064

Cited by 16 publications

(21 citation statements)

References 51 publications

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“…7H), perhaps because of the chronicity of the diet. Our finding that c-Fos-positive neurons in the PVN were increased by a LS diet is in agreement with a previous report in which the types of activated PVN cells were not differentiated (71). Similarly, c-Fos was increased in aldosterone-sensitive neurons of the NTS of rats on a chronic LS diet and decreased upon sodium repletion with a HS diet (25,28).…”

Section: Discussionsupporting

confidence: 93%

Expression of mineralocorticoid and glucocorticoid receptors in preautonomic neurons of the rat paraventricular nucleus

Chen

Gómez-Sánchez

Penman

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Activation of mineralocorticoid receptors (MR) of the hypothalamic paraventricular nucleus (PVN) increases sympathetic excitation. To determine whether MR and glucocorticoid receptors (GR) are expressed in preautonomic neurons of the PVN and how they relate to endogenous aldosterone levels in healthy rats, retrograde tracer was injected into the intermediolateral cell column at T4 to identify preautonomic neurons in the PVN. Expression of MR, GR, 11-␤ hydroxysteroid dehydrogenase1 and 2 (11␤-HSD1, 2), and hexose-6-phosphate dehydrogenase (H6PD) required for 11␤-HSD1 reductase activity was assessed by immunohistochemistry. RT-PCR and Western blot analysis were used to determine MR gene and protein expression. Most preautonomic neurons were in the caudal mediocellular region of PVN, and most expressed MR; none expressed GR. 11␤-HSD1, but not 11␤-HSD2 nor H6PD immunoreactivity, was detected in the PVN. In rats with chronic low or high sodium intakes, the low-sodium diet was associated with significantly higher plasma aldosterone, MR mRNA and protein expression, and c-Fos immunoreactivity within labeled preautonomic neurons. Plasma corticosterone and sodium and expression of tonicity-responsive enhancer binding protein in the PVN did not differ between groups, suggesting osmotic adaptation to the altered sodium intake. These results suggest that MR within preautonomic neurons in the PVN directly participate in the regulation of sympathetic nervous system drive, and aldosterone may be a relevant ligand for MR in preautonomic neurons of the PVN under physiological conditions. Dehydrogenase activity of 11␤-HSD1 occurs in the absence of H6PD, which regenerates NADP ϩ from NADPH and may increase MR gene expression under physiological conditions. mineralocorticoid receptor; aldosterone; sympathetic nervous system; preautonomic neuron; paraventricular nucleus; glucocorticoid receptor; 11-␤ hydroxysteroid dehydrogenase; sodium THE RENIN-ANGIOTENSIN-ALDOSTERONE system (RAAS) and sympathetic nervous system (SNS) interact to maintain fluid, electrolyte, and hemodynamic homeostasis essential for terrestrial life where sodium intake is often limited. Both the RAAS and SNS are activated by a lowering sodium intake, adaptive mechanisms ensuring adequate blood pressure (17,51,52,60,64,104). The paraventricular nucleus (PVN), and the SNS were shown by ablation studies to have a crucial role in mineralocorticoid-salt excess models of hypertension (6, 58). Chronic systemic aldosterone excess, as well as the intracerebroventricular infusion of aldosterone administered at concentrations too low to be effective when infused systemically, increase blood pressure and SNS activity (35,61). In both models, the hypertension and sympathetic activation are prevented by the intracerebroventricular infusion of mineralocorticoid receptor (MR) antagonists at doses lower than the effective dose infused peripherally (35,39,61). Xue et al. (108) reproduced these pharmacological results with the intracerebroventricular infusion of MR siRNA (108).The ...

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Section: Discussionsupporting

confidence: 93%

Expression of mineralocorticoid and glucocorticoid receptors in preautonomic neurons of the rat paraventricular nucleus

Chen

Gómez-Sánchez

Penman

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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“…As previously described by Hindmarch et al (6), nesfatin-1/NucB2 is expressed not only in the SON and PVN but also in the subfornical organ (SFO), as demonstrated by in situ hybridization histochemistry (ISH) and immunohistochemistry (IHC). The SFO, SON, and PVN have been recognized as regulators of body fluid homeostasis and sodium appetite (2,4,9,15,32). Thus, nesfatin-1/NucB2 may be involved not only in feeding behavior but also in body fluid regulation, as previously reported (11,29).…”

supporting

confidence: 52%

A role of nesfatin-1/NucB2 in dehydration-induced anorexia

Yoshimura

Matsuura

Ohkubo

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Nesfatin-1/NucB2, an anorexigenic molecule, is expressed mainly in the hypothalamus, particularly in the supraoptic nucleus (SON) and the paraventricular nucleus (PVN). Nesfatin-1/NucB2 is also expressed in the subfornical organ (SFO). Because the SON and PVN are involved in body fluid regulation, nesfatin-1/NucB2 may be involved in dehydration-induced anorexia. To clarify the effects of endogenous nesfatin-1/NucB2, we studied changes in nesfatin-1/NucB2 mRNA levels in the SFO, SON, and PVN in adult male Wistar rats after exposure to osmotic stimuli by using in situ hybridization histochemistry. Significant increases in nesfatin-1/NucB2 mRNA levels, ∼2- to 3-fold compared with control, were observed in the SFO, SON, and PVN following water deprivation for 48 h, consumption of 2% NaCl hypertonic saline in drinking water for 5 days, and polyethylene glycol-induced hypovolemia. In addition, nesfatin-1/NucB2 expression was increased in response to water deprivation in a time-dependent manner. These changes in nesfatin-1/NucB2 mRNA expression were positively correlated with plasma sodium concentration, plasma osmolality, and total protein levels in all of the examined nuclei. Immunohistochemistry for nesfatin-1/NucB2 revealed that nesfatin-1/NucB2 protein levels were also increased after 48 h of dehydration and attenuated by 24 h of rehydration. Moreover, intracerebroventricular administration of nesfatin-1/NucB2-neutralizing antibody after 48 h of water deprivation resulted in a significant increase in food intake compared with administration of vehicle alone. These results suggested that nesfatin-1/NucB2 is a crucial peptide in dehydration-induced anorexia.

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“…Regarding saline intake ratio, our results corroborate the observations of Stricker et al . and Lu et al . who describe an increased saline intake ratio in rats chronically deprived of sodium for 8 or 14 days.…”

Section: Discussionmentioning

confidence: 93%

The Role of Angiotensin II on Sodium Appetite After a Low‐Sodium Diet

Mecawi

Vilhena‐Franco

Fonseca

et al. 2013

J Neuroendocrinology

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The present study aimed to investigate the role of angiotensin II (Ang II) on sodium appetite in rats subjected to a normal or a low-sodium diet (1% or > 0.1% NaCl) for 4 days. During sodium restriction, a reduction in water intake, urinary volume and sodium excretion was observed. After a low-sodium diet, we observed decreased plasma protein concentrations and haematocrit associated with a slight reduction in arterial pressure, without any significant changes in heart rate, natraemia, corticotrophin-releasing hormone mRNA expression in the paraventricular nucleus and corticosterone levels. After providing hypertonic saline, there was an increase in saline intake followed by a small increase in water intake, resulting in an enhanced saline intake ratio and the recovery of arterial pressure. Sodium deprivation increased plasma but not brain Ang I and II concentrations. A low-sodium diet increased kidney renin and liver angiotensinogen mRNA levels but not lung angiotensin-converting enzyme mRNA expression. Moreover, Ang II type 1a receptor mRNA expression was increased in the subfornical organ and the dorsal raphe nucleus and decreased in the medial preoptic nuclei, without changes in the paraventricular nucleus and the nucleus of solitary tract after a low-sodium diet. Blockade of AT(1) receptors or brain Ang II synthesis led to a reduction in sodium intake after a low-sodium diet. Intracerebroventricular injection of Ang II led to a similar increase in sodium and water intake in the control and low-sodium diet groups. In conclusion, the results of the present study suggest that Ang II is involved in the increased sodium appetite after a low-sodium diet.

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Dietary sodium deprivation evokes activation of brain regional neurons and down-regulation of angiotensin II type 1 receptor and angiotensin-convertion enzyme mRNA expression

Cited by 16 publications

References 51 publications

Expression of mineralocorticoid and glucocorticoid receptors in preautonomic neurons of the rat paraventricular nucleus

Expression of mineralocorticoid and glucocorticoid receptors in preautonomic neurons of the rat paraventricular nucleus

A role of nesfatin-1/NucB2 in dehydration-induced anorexia

The Role of Angiotensin II on Sodium Appetite After a Low‐Sodium Diet

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