Regulation of angiotensinogen gene expression in the rat forebrain by adrenal steroids and relation to salt appetite

Riftina, Faina; Angulo, Jesús A.; Pompei, Pierluigi; McEwen, Bruce S.

doi:10.1016/0169-328x(95)00114-8

Cited by 22 publications

(13 citation statements)

References 35 publications

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“…In this study, the increase in AT1 binding in the SFO following DOCA + DEX treatment paralleled the increase in salt appetite, suggesting that these nuclei would be especially sensitive to brain AngII. Because intracerebroventricular administration of AngII leads to an exaggerated salt appetite following steroid treatment [8, 9], and because DEX can increase the expression of angiotensinogen [17, 18, 19, 20], future studies will examine if salt and water intake are further enhanced in DOCA + DEX treatment by intracerebroventricular AngII challenge or from locally produced AngII-activating AT1 receptors. Also, since the increase in AT1 binding required the combined actions of DOCA and DEX, the SFO (and area postrema) may represent a site where DEX augmented the actions of DOCA by increasing MR [21].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Mineralocorticoids and Glucocorticoids Cooperatively Increase Salt Intake and Angiotensin II Receptor Binding in Rat Brain

Shelat

King²,

Flanagan‐Cato³

et al. 1999

Neuroendocrinology

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Mineralocorticoids, such as deoxycorticosterone acetate (DOCA), and angiotensin II (AngII) act synergistically in the brain to elicit salt appetite. Glucocorticoids, such as dexamethasone (DEX), also may enhance the behavioral effects of DOCA and AngII. However, the brain regions involved in these behavioral interactions have not been elucidated. This study tested the hypothesis that DEX potentiates the effects of DOCA on AngII binding, especially at the AT1 receptor. We confirmed that DEX potentiated the effects of DOCA on salt appetite. Concomitantly, steroid-specific and region-specific changes in AT1 binding were noted. Specifically, in the hypothalamic paraventricular nucleus, treatment with DEX or DOCA + DEX increased AT1 binding. In the subfornical organ (SFO) and area postrema, there was an increase in AT1 binding when both steroids were combined, but not when given individually. However, there was no change in AT2 binding in any brain region studied and no change in AT1 or AT2 binding to either receptor subtype in the pituitary. The results indicate that DOCA and DEX may increase the sensitivity of the brain to the behavioral and physiological actions of AngII by upregulating AT1 receptors in the SFO and area postrema.

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Section: Discussionmentioning

confidence: 99%

“…Glucocorticoids increase the expression of brain angiotensinogen [17, 18, 19, 20], which may increase the production of AngII. Second, glucocorticoids stimulate the expression of MR [21], which could explain how glucocorticoids augment the salt appetite seen in mineralocorticoid-treated rats [22].…”

Section: Discussionmentioning

confidence: 99%

Mineralocorticoids and Glucocorticoids Cooperatively Increase Salt Intake and Angiotensin II Receptor Binding in Rat Brain

Shelat

King²,

Flanagan‐Cato³

et al. 1999

Neuroendocrinology

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“…Adrenal steroids regulate multiple components of the renin-angiotensin system, including angiotensinogen (Deschepper & Flaxman 1990, Bunnemann et al 1993, Riftina et al 1995, Ryan et al 1997) and angiotensinconverting enzyme (Mendelsohn et al 1982), both of which could generate more AngII ligand. In addition, the physiological and behavioral actions of AngII can be modulated by mineralocorticoids (Epstein 1982, Fluharty & Epstein 1983, Zhang et al 1984, Wilson et al 1986, King et al 1988 and glucocorticoids (Krakoff et al 1975, Whitworth 1987, Ganesan & Sumners 1989, Sumners et al 1991 at the level of the AT1 receptor (Schiffrin et al 1984, Wilson et al 1986, Sumners & Fregly 1989, Ullian et al 1992.…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoid and mineralocorticoid regulation of angiotensin II type 1 receptor binding and inositol triphosphate formation in WB cells

Shelat¹,

Flanagan-Cato²,

Sj³

1999

Journal of Endocrinology

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Mineralocorticoids, glucocorticoids, and angiotensin II (AngII) act cooperatively to maintain body fluid homeostasis. Mineralocorticoids, such as aldosterone and deoxycorticosterone-acetate (DOCA), function synergistically with AngII in the brain to increase salt appetite and blood pressure. In addition, glucocorticoids increase AngII-induced drinking and pressor responses and may also facilitate the actions of aldosterone on salt appetite. The AngII Type 1 (AT1) receptor mediates many of the physiological and behavioral actions of AngII. This receptor is coupled to the G-protein Gq, which mediates AngII-induced inositol triphosphate (IP3) formation. The WB cell line, a liver epithelial cell line that expresses the AT1 receptor, was used to examine the cellular basis of glucocorticoid and mineralocorticoid regulation of AT1 function. In this study corticosterone and dexamethasone treatments increased the number of AT1 receptors by activating the glucocorticoid receptor (GR). This increase in AT1 binding resulted in enhanced AngII-stimulated IP3 formation. However, only supraphysiological doses of aldosterone or DOCA increased AT1 binding, and this effect also was mediated by GR activation. Furthermore, despite evidence that mineralocorticoids and glucocorticoids function together to increase AngII-stimulated actions in vivo, aldosterone and dexamethasone did not act synergistically to affect AT1 binding, Gq expression, or IP3 formation. These results indicate that GR activation, and the subsequent increases in AT1 binding and in AngII-stimulated IP3 formation, may represent a cellular mechanism underlying the synergy between adrenal steroids and AngII.

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“…80 GR agonists also increase the production of brain angiotensinogen. 78 This could raise Ang II and produce an effect similar to that observed when aldosterone and Ang II are administered together.…”

Section: Blood Pressure Effectsmentioning

confidence: 99%

“…Systemic administration of aldosterone, but not GR agonists, restores sodium appetite to normal. 78 Inhibition of MR production through the injection of antisense oligonucleotides into the rat brain suggests that the sodium appetite response involves glucocorticoid-selective MR in the amygdala where 11β-HSD2 is expressed. 71,79 Although GR agonists alone do not affect salt appetite, in combination with mineralocorticoids they increase salt appetite to a greater extent than mineralocorticoids alone.…”

Section: Blood Pressure Effectsmentioning

confidence: 99%

Local renin-angiotensin systems and their interactions with extra-adrenal corticosteroid production

MacKenzie

Fraser

Connell

et al. 2002

J Renin Angiotensin Aldosterone Syst

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Adrenal aldosterone production is regulated by the renin-angiotensin system (RAS). It is now known that several other tissues are capable of extra-adrenal aldosterone biosynthesis and that these tissues can also generate angiotensin II through local RAS. Therefore, the regulation of local aldosterone production by the local RAS is a distinct possibility. In this review, we present evidence for the existence of such systems in the vascular system, heart and brain. We then discuss the possibility of interactions between the RAS and aldosterone synthesis at the local level and speculate on the possible physiological effects of such systems in these tissues.

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Regulation of angiotensinogen gene expression in the rat forebrain by adrenal steroids and relation to salt appetite

Cited by 22 publications

References 35 publications

Mineralocorticoids and Glucocorticoids Cooperatively Increase Salt Intake and Angiotensin II Receptor Binding in Rat Brain

Mineralocorticoids and Glucocorticoids Cooperatively Increase Salt Intake and Angiotensin II Receptor Binding in Rat Brain

Glucocorticoid and mineralocorticoid regulation of angiotensin II type 1 receptor binding and inositol triphosphate formation in WB cells

Local renin-angiotensin systems and their interactions with extra-adrenal corticosteroid production

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