Aldosteronism revisited: Perspectives on less well-recognized actions of aldosterone

Weber, Karl T.

doi:10.1016/s0022-2143(03)00062-3

Cited by 47 publications

(35 citation statements)

References 119 publications

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“…3). A series of recent studies further revealed that increased expression of pro-inflammatory genes, such as VCAM-1, COX-2, and osteopontin, are preceded by 'aldosterone-induced vasculitis' [30,36,70]. We have also demonstrated that physiological concentrations of aldosterone (as low as 10 -10 M) directly acts on endothelial cells to induce osteopontin gene expression through the non-epithelial MR activation [71].…”

Section: Mr Activation and Cardiovascular Injurymentioning

confidence: 66%

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Aldosterone as a Cardiovascular Risk Hormone

Yoshimoto

Hirata

2007

Endocr J

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Abstract. The pathophysiological role of aldosterone in the development of cardiovascular disease has long been considered to be due its potent volume expansion/hypertensive effect mainly via mineralocorticoid receptor (MR) expressed in renal tubular epithelial cells. However, recent accumulating lines of evidence from clinical and experimental studies have suggested that direct cardiovascular effect of aldosterone contributes to the development of cardiovascular injury via MRs in non-epithelial tissue. A series of recent clinical studies have revealed that patients with primary aldosteronism have higher incidence of cardiovascular and renal complications than those with essential hypertension, and that aldosterone antagonism has cardiovascular protective effect in patients with heart failure independent from blood pressure. Numerous experimental studies have shown that both inflammation and oxidative stress play an initial and key role in the development of aldosterone-induced cardiovascular injury via non-epithelial MR activation. In this review, we discuss recent research progress in aldosterone and MR effects, with special emphasis on the pathophysiological role of aldosterone in cardiovascular diseases and the possible molecular mechanism(s) of cardiovascular injury by non-epithelial MR activation.

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Section: Mr Activation and Cardiovascular Injurymentioning

confidence: 66%

“…However, numerous lines of evidence have emerged to support the direct role of aldosterone in cardiovascular injury through the mechanism independent of its salt-water retention and hypertensive effects [15,16,30].…”

Section: Evidence From Experimental Animal Modelsmentioning

confidence: 99%

Aldosterone as a Cardiovascular Risk Hormone

Yoshimoto

Hirata

2007

Endocr J

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“…Aldosterone is actively involved in producing CSF volume and composition, as well as in the regulation of blood pressure. As the renin-aldosterone system is activated in GS, aldosterone levels in the CSF as well as in plasma will increase, and stimulate the net transport and reabsorption of sodium/potassium across the epithelium in the choroidal plexus, and thus may be involved in the increased production of CSF (5,13).…”

Section: Discussionmentioning

confidence: 99%

A Case of Gitelman Syndrome Associated with Idiopathic Intracranial Hypertension

et al. 2011

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An 18-year-old woman with Gitelman syndrome (GS) associated with idiopathic intracranial hypertension (IIH) is described. She was obese and showed a 10 kg gain in body weight over a period of 8 months. She presented with headache, vomiting, and diplopia. She had bilateral papilledema, and right abducens palsy. CSF examination demonstrated high pressure (over 320 mmH2O) with normal cytochemistry. Brain MRI was normal. She showed mild alkalosis, hypokalemia, hypomagnesemia, increased plasma renin activity, and normal blood pressure. Two heterozygous mutations in the SLC12A3 gene were identified. Therefore, she was diagnosed as GS with IIH. We should keep in mind the possible occurrence of IIH in GS.

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“…We and other investigators have shown that increased proinflammatory gene expression in vascular tissue is a hallmark of Aldoinduced cardiovascular injury. 4,29,30 This study clearly showed that CILO almost completely blocked the upregulation of aortic proinflammatory gene expressions, including osteopontin, MCP-1, PDGF-A, ICAM-1, MMP-2 and ACE, in Aldo-induced hypertension. Our results are partly in agreement with those of the inhibition of aortic vascular cell adhesion molecule-1 and MCP-1 expression by CILO in vivo 16 and in vitro.…”

Section: Discussionmentioning

confidence: 54%

Vasculoprotective effect of cilostazol in aldosterone-induced hypertensive rats

et al. 2009

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Cilostazol (CILO), a selective inhibitor of phosphodiesterase 3 with potent antithrombotic property, has been shown to have a vasculoprotective effect in atherosclerosis animal models due to its potential anti-inflammatory and antioxidant actions. This study was undertaken to investigate whether CILO has in fact any vasculoprotective effects in aldosterone-induced hypertensive rats (Aldo-rats), and whether CILO affects Aldo-induced oxidative stress, nitric oxide (NO) production and pro-inflammatory gene expression. Treatment with CILO markedly ameliorated perivascular inflammatory changes in the coronary arterioles of Aldo-rats without affecting the systolic blood pressure and left ventricular weight. Treatment with CILO also prevented the increase in plasma levels of thiobarbituric acid-reactive substances, an oxidative stress marker, as well as decreased urinary NOx excretion in Aldo-rats. Furthermore, CILO almost completely inhibited a set of upregulated proinflammatory genes (ICAM-1, MCP-1, PDGF-A, osteopontin, MMP-2 and ACE), as well as NAD(P)H oxidase components (p22phox, gp91phox, p47phox) and Aldoinducible genes (SGK-1 and NHE-1) in the aortic tissues from Aldo-rats. Taken together, this study showed for the first time that CILO prevented Aldo-induced vascular inflammation and injury without affecting the blood pressure, suggesting its vasculoprotective effect on Aldo-induced vascular injury independent of blood pressure.

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Aldosteronism revisited: Perspectives on less well-recognized actions of aldosterone

Cited by 47 publications

References 119 publications

Aldosterone as a Cardiovascular Risk Hormone

Aldosterone as a Cardiovascular Risk Hormone

A Case of Gitelman Syndrome Associated with Idiopathic Intracranial Hypertension

Vasculoprotective effect of cilostazol in aldosterone-induced hypertensive rats

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