Aldosterone and cardiovascular risk

Vogt, Bruno; Burnier, Michel

doi:10.1007/s11906-009-0076-8

Cited by 19 publications

(21 citation statements)

References 50 publications

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“…Treatment with MR antagonists decreases both cardiovascular risk markers and insulin resistance even in insulin-dependent diabetics (260, 440, 463, 503). Aldosterone may have a primary or amplifying role in the Cardiometabolic Syndrome.…”

Section: Pathophysiological Implications Of Inappropriate Mr Activationmentioning

confidence: 99%

The Multifaceted Mineralocorticoid Receptor

Gómez-Sánchez

2014

Comprehensive Physiology

277

224

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The primary adrenal cortical steroid hormones, aldosterone, and the glucocorticoids cortisol and corticosterone, act through the structurally similar mineralocorticoid (MR) and glucocorticoid receptors (GRs). Aldosterone is crucial for fluid, electrolyte, and hemodynamic homeostasis and tissue repair; the significantly more abundant glucocorticoids are indispensable for energy homeostasis, appropriate responses to stress, and limiting inflammation. Steroid receptors initiate gene transcription for proteins that effect their actions as well as rapid non-genomic effects through classical cell signaling pathways. GR and MR are expressed in many tissues types, often in the same cells, where they interact at molecular and functional levels, at times in synergy, others in opposition. Thus the appropriate balance of MR and GR activation is crucial for homeostasis. MR has the same binding affinity for aldosterone, cortisol, and corticosterone. Glucocorticoids activate MR in most tissues at basal levels and GR at stress levels. Inactivation of cortisol and corticosterone by 11β-HSD2 allows aldosterone to activate MR within aldosterone target cells and limits activation of the GR. Under most conditions, 11β-HSD1 acts as a reductase and activates cortisol/corticosterone, amplifying circulating levels. 11β-HSD1 and MR antagonists mitigate inappropriate activation of MR under conditions of oxidative stress that contributes to the pathophysiology of the cardiometabolic syndrome; however, MR antagonists decrease normal MR/GR functional interactions, a particular concern for neurons mediating cognition, memory, and affect.

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Section: Pathophysiological Implications Of Inappropriate Mr Activationmentioning

confidence: 99%

The Multifaceted Mineralocorticoid Receptor

Gómez-Sánchez

2014

Comprehensive Physiology

277

224

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“…Although aldosterone's classic effect is attributed to mineralocorticoid receptor (MR)-mediated salt and fluid retention and to the regulation of blood pressure homeostasis (Connell and Davies, 2005;Jansen et al, 2009;Vogt and Burnier, 2009), it can also induce ''non-genomic'' effects independent of MR activation (Lösel et al, 2004;Mihailidou and Funder, 2005). We have discovered that aldosterone, which stimulates collagen production in human heart-derived myofibrolasts via MR activation, also induces elastogenesis in an MR-independent manner (Bunda et al, 2007(Bunda et al, , 2009.…”

Section: Introductionmentioning

confidence: 99%

Aldosterone and Mineralocorticoid Receptor Antagonists Modulate Elastin and Collagen Deposition in Human Skin

Mitts

Bunda

Wang

et al. 2010

Journal of Investigative Dermatology

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We have shown that the steroid hormone aldosterone, recognized for its action on the kidney and the cardiovascular system, also modulates deposition of extracellular matrix in human skin. We have shown that treatment of primary cultures of normal skin fibroblasts with aldosterone (10 n-1 μM), in addition to stimulation of collagen type I expression, induces elastin gene expression and elastic fiber deposition. We have further shown that the elastogenic effect of aldosterone, which can be enhanced in the presence of mineralocorticoid receptor (MR) antagonists spironolactone and eplerenone, is executed in a MR-independent manner via amplification of IGF-I receptor-mediated signaling. Because aldosterone applied alone stimulates both collagen and elastin deposition in cultures of fibroblasts and in cultures of skin explants derived from dermal stretch marks, we postulate that this steroid should be used in the treatment of damaged skin that loses its volume and elasticity. Moreover, aldosterone applied in conjunction with spironolactone or eplerenone induces matrix remodeling and exclusively enhances elastogenesis in cultures of fibroblasts and explants derived from dermal scars and keloids. We therefore propose that intra-lesional injection of these factors should be considered in therapy for disfiguring dermal lesions and especially in prevention of their recurrence after surgical excision.

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“…RAAS acts in a paracrine/ autocrine manner and is of great significance in maintaining homeostasis in functions and structure of cardiovascular system [19]. As an essential hormone in the RAAS system [18], ALD promotes collagen deposition and fibrosis, thus leading to fibrosis and structural remodeling of the heart [20]. In this study, we found that the mRNA expression of ALD precursor, CYP11B2, in the peri-infarcted zone was increased after the left anterior descending coronary artery was occluded.…”

Section: Discussionmentioning

confidence: 99%

Effects of intermedin1-53 on myocardial fibrosis

Yang¹,

Zhang²,

Jia³

et al. 2013

ABBS

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Intermedin (IMD) is a member of the calcitonin/calcitonin gene-related peptide (CGRP) family and has similar or more potent cardiovascular actions than adrenomedullin (ADM) and any other CGRP. The aim of the present work is to study the effects of IMD1-53 on cardiac fibroblast fibrosis in vivo and in vitro. Myocardial infarction model was prepared by ligating rats' left anterior descending coronary artery. Mesenchymal collagen contents in the left ventricle were accessed by Sirius-red stain. Heart functions were explored by hemodynamic changes. Expression of I and III type collagens, IMD1-53, receptor activity-modifying proteins (RAMP)1/2/3, and calcitonin receptor-like receptor (CRLR) in left ventricle were detected by western blot analysis. Cardiac fibroblasts (CFbs) fibrosis was induced by treating the cells with aldosterone (ALD). CFbs proliferation and the hydroxyproline contents in supernatants were determined by 3-[4,5-dimehyl-2-thiazolyl]-2,5-diphenyl-2H-tetrazolium bromide assay and enzyme-linked immunosorbent assay. Heart function was decreased in myocardial infarction model rats. Expression of type I and type III collagens in infarcted zone in myocardial rats was higher than those in the sham-operated group. IMD1-53, RAMP, and CRLR in left ventricle were also up-regulated. In vitro experiment showed that ALD was a powerful stimulator of CFbs activation. IMD1-53 decreased ALD-induced CFbs proliferation in a dose-dependent manner. Moreover, CGRP8-37 and ADM22-52 remarkably blocked the effect of IMD1-53 on ALD-induced myocardial cell fibrosis. IMD could be involved in the onset of cardiac fibrosis. Like ADM, IMD1-53 exerts an antifibrotic effect on CFbs, which might be mediated by CRLR/RAMP complex and ADM receptor.

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Aldosterone and cardiovascular risk

Cited by 19 publications

References 50 publications

The Multifaceted Mineralocorticoid Receptor

The Multifaceted Mineralocorticoid Receptor

Aldosterone and Mineralocorticoid Receptor Antagonists Modulate Elastin and Collagen Deposition in Human Skin

Effects of intermedin1-53 on myocardial fibrosis

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