Aldosterone in the brain

Geerling, Joel C.; Loewy, A.

doi:10.1152/ajprenal.90399.2008

Cited by 160 publications

(161 citation statements)

References 199 publications

(310 reference statements)

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“…Aldosterone, another natriorexigenic hormone, is known to be detected by 11β-hydroxysteroid dehydrogenase type 2 (HSD2)-positive neurons in the nucleus of the solitary tract (NTS) and to induce salt appetite (Geerling and Loewy, 2009). …”

Section: Iii4 Discussionmentioning

confidence: 99%

Distinct neural mechanisms for the control of thirst and salt appetite in the subfornical organ

et al. 2016

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Section: Iii4 Discussionmentioning

confidence: 99%

Distinct neural mechanisms for the control of thirst and salt appetite in the subfornical organ

et al. 2016

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“…12 However, the enzymes for steroid biosynthesis are present in the central nervous system 41 and RVLM, 15 and aldosterone can be detected in the tissues of various brain regions in vitro 41 and in vivo. 42 In particular, it should be noted that Gomez-Sanchez et al reported that aldosterone was detectable in the whole brain of adrenalectomized rats, despite the fact that plasma aldosterone was undetectable.…”

Section: Discussionmentioning

confidence: 99%

“…11 Recent studies have reported the distribution of MRs or ENaCs in the choroid plexus, ependyma and neurons, such as those in the supraoptic nucleus, paraventricular nucleus and nucleus tractus solitarius. 12,13 In addition, the expression of MR mRNA has been reported in the brainstem, 14 including the rostral ventrolateral medulla (RVLM) and caudal ventrolateral medulla. 15,16 These findings suggest that MRs in the central nervous system, especially in neurons, regulate Na + influx via ENaCs, leading to hypertension and sympathoexcitation.…”

Section: Introductionmentioning

confidence: 99%

Activation of mineralocorticoid receptors in the rostral ventrolateral medulla is involved in hypertensive mechanisms in stroke-prone spontaneously hypertensive rats

et al. 2012

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Mineralocorticoid receptor (MR) is recognized as a target for therapeutic intervention in hypertension and heart failure. MRs in the central nervous system are thought to have an important role in blood pressure regulation. Thus, we examined whether activation of the MR pathway in the rostral ventrolateral medulla (RVLM) of the brainstem contributes to the neural mechanism of hypertension in stroke-prone spontaneously hypertensive rats (SHRSPs). We microinjected eplerenone, aldosterone or Na + -rich artificial cerebrospinal fluid (aCSF) into the RVLM of anesthetized Wistar-Kyoto (WKY) rats and SHRSPs. Arterial pressure (AP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were recorded. The expressions of the MR protein and the serumand glucocorticoid-regulated kinase protein (Sgk1), which is a marker of MR activity, in the RVLM were measured by western blot analysis. Bilateral microinjection of eplerenone into the RVLM decreased AP and RSNA in WKY rats and SHRSPs, and the decreases in those variables were significantly greater in SHRSPs than WKY rats. Microinjection of aldosterone or Na + -rich aCSF into the RVLM increased AP and RSNA dose-dependently. The increases in those variables were significantly greater in SHRSPs than in WKY rats. The pressor responses of aldosterone or Na + -rich aCSF were attenuated by the prior injection of eplerenone in SHRSPs. Sgk1 expression levels in the RVLM were significantly greater in SHRSPs than in WKY rats. These findings suggest that activation of MRs in the RVLM enhances sympathetic activity, thereby contributing to the neural mechanism of hypertension in the SHRSP.

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Section: Glucocorticoid Receptorsmentioning

confidence: 99%

“…Both MR and GC receptors mediate rapid non-genomic effects via the binding of cortisol to cell membranes [86] . In the CNS, MRs bind very low levels of GCs in vivo [87,88] against the 100-1000-fold molar excess of GCs that circulate in the blood [85] .The acute effects of GCs on target cells in the HPA axis are predominantly mediated via their rapid action at their receptor sites. This action produces a rapid negative feedback response of the HPA axis that suppresses its own stress-induced hyperactivity.…”

mentioning

confidence: 99%

Hypothalamic-pituitary-adrenal axis function during perinatal depression

et al. 2015

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Abnormal function of the hypothalamic-pituitary-adrenal (HPA) axis is an important pathological finding in pregnant women exhibiting major depressive disorder. They show high levels of cortisol proinflammatory cytokines, hypothalamic-pituitary peptide hormones and catecholamines, along with low dehydroepiandrosterone levels in plasma. During pregnancy, the TH2 balance together with the immune system and placental factors play crucial roles in the development of the fetal allograft to full term. These factors, when altered, may generate a persistent dysfunction of the HPA axis that may lead to an overt transfer of cortisol and toxicity to the fetus at the expense of reduced activity of placental 11β-hydroxysteroid dehydrogenase type 2. Epigenetic modifications also may contribute to the dysregulation of the HPA axis. Affective disorders in pregnant women should be taken seriously, and therapies focused on preventing the deleterious effects of stressors should be implemented to promote the welfare of both mother and baby.Keywords: brain; depression; neuroendocrine; pregnancy; stress; glucocorticoids Extensive studies have demonstrated that early life stressors produce changes in behavior and enhance the sensitivity of the stress response systems [1][2][3][4] . Although the genetic background has been implicated in the development of mood-related disorders, and genetic research has identified some chromosomal regions and genes that are involved in susceptibility to mood disorders, the etiology of anxiety and depressive disorders is still not clear in humans, particularly in women with major depressive disorder (MDD) [1] .The pathogenesis of perinatal depression is an emerging field. Although considerable progress has been made in this area in the last few years, there still remain unanswered questions and gaps in our knowledge of the underlying pathogenesis, the long-term impact of perinatal depression on the developing fetus, and the best methods for counseling pregnant women concerning the risks of untreated MDD versus the risks of psychopharmacologic treatment during pregnancy and lactation [5] . Meta-analysis studies have reported that the mean prevalence rate of prenatal depression is ~12% (this varies greatly according to location, mode of assessment, and socioeconomic conditions), and show that a large percentage of pregnant women displaying major depression remain depressed in the postpartum period and/or continuously [6,7] . Anxiety, depressive disorder, and stress during pregnancy are risk Phillipe Leff Gelman, et al. HPA axis in perinatal depression 339 factors for negative outcomes in newborns, like preterm birth or low birth weight; also, insecure attachment and impaired child development could be a consequence of mental disorders during pregnancy [6,[8][9][10] . The mechanisms by which maternal depression impacts fetal and neonatal development are currently under investigation; there is some evidence that depressive symptoms impact the infant's hypothalamic-pituitary-adrenal (HPA) axis, enhancing the ...

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Aldosterone in the brain

Cited by 160 publications

References 199 publications

Distinct neural mechanisms for the control of thirst and salt appetite in the subfornical organ

Distinct neural mechanisms for the control of thirst and salt appetite in the subfornical organ

Activation of mineralocorticoid receptors in the rostral ventrolateral medulla is involved in hypertensive mechanisms in stroke-prone spontaneously hypertensive rats

Hypothalamic-pituitary-adrenal axis function during perinatal depression

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