Neointimal thickening after balloon denudation is enhanced by aldosterone and inhibited by spironolactone, and aldosterone antagonist

Belle, Éric Van; Bauters, Christophe; Wernert, Nicolas; Hamon, Martial; McFadden, Eugène; Racadot, A; Dupuis, B; Lablanche, Jean‐Marc; Bertrand, Michel E.

doi:10.1016/s0008-6363(96)88542-7

Cited by 49 publications

(23 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Animal studies have shown that aldosterone, acting via MR, exacerbates vascular injury responses to a variety of conditions that cause endothelial dysfunction, including mechanical EC injury (13,14,16), uninephrectomy/high salt-induced hypertension (15), or hyperlipidemia-induced vascular damage (44). Our carotid injury model suggests that the detrimental vascular effects of aldosterone occur only with the concomitant presence of endothelial injury, but the ex vivo experiments demonstrate that aldosterone upregulates PGF expression even in normal vessels (Figure 2).…”

Section: Figurementioning

confidence: 99%

“…First, the wire carotid injury model was chosen for these studies because it is a reproducible method for examining the in vivo mechanisms regulating medial VSMC proliferation and fibrosis. However, aldosterone also has been shown to contribute to neointima formation (13,16) and atherogenesis (44), processes that will need to be explored in distinct animal models. Although the molecular mechanism of aldosterone's contribution to neointima formation remains unknown (13,16), the pathways controlling SMC proliferation in the media and the intima likely overlap, and hence the MR/PGF/Flt1 pathway may also play a role in intimal SMC proliferation, although this remains to be formally tested.…”

Section: Figurementioning

confidence: 99%

“…Animal studies in rat, rabbit, and pig models demonstrate that aldosterone infusion in vivo enhances vascular remodeling in response to endothelial damage or dysfunction (13)(14)(15). The vascular effects of aldosterone are reversed by aldosterone antagonists, implicating MR in the mechanism (16), although the role of vascular versus renal MR in these models is unclear. In humans, increased carotid artery thickening is associated with electrolyte evidence of aldosterone excess (7), and inhibition of the angiotensin-aldosterone pathway slows progression of carotid remodeling (17).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Placental growth factor mediates aldosterone-dependent vascular injury in mice

Jaffe¹,

Newfell²,

Aronovitz³

et al. 2010

J. Clin. Invest.

View full text Add to dashboard Cite

Section: Figurementioning

confidence: 99%

Section: Figurementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Placental growth factor mediates aldosterone-dependent vascular injury in mice

Jaffe¹,

Newfell²,

Aronovitz³

et al. 2010

J. Clin. Invest.

View full text Add to dashboard Cite

“…ALDO is extracted by the chronically failing human heart of diverse aetiological origins, a response blocked by spironolactone. 127 Under circumstances in which circulating ALDO is not increased, spironolactone attenuates neointimal thickening following vascular barotrauma, 128 tissue repair at sites of fibrous tissue formation 129 and vascular injury in stroke-prone rats. 130 These observations further suggest that auto/paracrine properties of locally-produced ALDO participate in tissue repair.…”

Section: Central Actions Of Aldosteronementioning

confidence: 99%

Toward a broader understanding of aldosterone in congestive heart failure

Weber

Sun

Wodi

et al. 2003

J Renin Angiotensin Aldosterone Syst

View full text Add to dashboard Cite

Discovered some 50 years ago, aldosterone (ALDO) has come to be recognised as a mineralocorticoid hormone with well-known endocrine properties in epithelial cells that contribute to the pathophysiology of congestive heart failure. This includes Na + in such non-epithelial cells as peripheral blood mononuclear cells; its influence on endothelial cell function; and its central actions that involve regulation of cerebrospinal fluid composition produced by epithelial cells of the choroid plexus, activity of the hypothalamic paraventricular nucleus involved in Na + appetite, Na + and H 2 O excretion and sympathetic nerve activity, and the regulation of TNF-α production from central and/or peripheral sources. Extra-adrenal steroidogenesis and auto/paracrine properties of ALDO generated de novo in the cardiovasculature are now under investigation and preliminary findings suggest they contribute to tissue repair. The past decade has witnessed a revival of interest in this steroid molecule. In years to come, an even broader understanding of ALDO's contribution to the pathophysiology of congestive heart failure will undoubtedly emerge.

show abstract

“…Endothelial dysfunction is one of the factors of atherosclerosis. Aldosterone exacerbates neointimal thickening after balloon injury and is blocked by spironolactone [30]. Aldosterone has been reported to induce a prothrombotic condition by upregulation of plasminogen activator inhibitor-1 [31].…”

Section: Mechanismsmentioning

confidence: 99%

Mineralocorticoid receptor antagonists in dialysis patients

et al. 2016

View full text Add to dashboard Cite

Mineralocorticoid receptor (MR) antagonists are known to have beneficial effects in patients with cardiovascular disease without renal failure. However, there have been few published studies on the effectiveness of MR antagonists in dialysis patients, and most of the studies were small-sized. The present review focuses on the effectiveness of MR antagonists and the risk of hyperkalemia in dialysis patients. Severe hyperkalemia due to treatment with MR antagonists in dialysis patients is not common, particularly in peritoneal dialysis (PD) patients, and the prospect of cardioprotective effects has been hopeful in both hemodialysis (HD) and PD patients. Further studies are required to establish optimal protocols for the use of MR antagonists in these patients without adverse effects.

show abstract

Neointimal thickening after balloon denudation is enhanced by aldosterone and inhibited by spironolactone, and aldosterone antagonist

Cited by 49 publications

References 0 publications

Placental growth factor mediates aldosterone-dependent vascular injury in mice

Placental growth factor mediates aldosterone-dependent vascular injury in mice

Toward a broader understanding of aldosterone in congestive heart failure

Mineralocorticoid receptor antagonists in dialysis patients

Contact Info

Product

Resources

About