Aldosterone and Vascular Inflammation

Brown, Nancy J.

doi:10.1161/hypertensionaha.107.095489

Cited by 214 publications

(198 citation statements)

References 105 publications

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“…This rapid effect suggests that aldosterone is signaling through previously synthesized messengers, rather than by regulating the transcription of proteins. Our data add to the growing literature describing rapid, nongenomic effects of aldosterone (2,5,(32)(33)(34)(35). For example, aldosterone activates signaling pathways such as PKA, PKC, PKD, MAPK, and the NADPH oxidase in vascular smooth muscle; and aldosterone activates phosphatidylinositol 3-kinase in endothelial cells (32,34,(36)(37)(38)(39)(40)(45)(46)(47).…”

Section: Aldosterone Activates Endothelial Exocytosis Through a Nongementioning

confidence: 52%

“…The mineralocorticoid receptor (MR) in epithelial cells lining the distal nephron mediates aldosterone regulation of electrolytes. However, aldosterone may have additional physiological effects, such as increasing fibrosis, modulating oxidative stress, and triggering vascular inflammation (1)(2)(3)(4)(5)(6)(7).…”

mentioning

confidence: 99%

“…Hyperaldosteronism is associated with vascular inflammation (1,2,(8)(9)(10)(11)(12)(13)(14). Aldosterone infusion induces leukocyte infiltration into arteries of rats and increases the expression of proinflammatory markers (15,16).…”

mentioning

confidence: 99%

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Aldosterone activates endothelial exocytosis

Jeong¹,

Chaupin²,

Matsushita³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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Although elevated levels of aldosterone are associated with vascular inflammation, the proinflammatory pathways of aldosterone are not completely defined. We now show that aldosterone triggers endothelial cell exocytosis, the first step in leukocyte trafficking. Exogenous aldosterone stimulates endothelial exocytosis of Weibel-Palade bodies, externalizing P-selectin and releasing von Willebrand factor. Spironolactone, a nonselective mineralocorticoid receptor (MR) blocker, antagonizes aldosterone-induced endothelial exocytosis. Knockdown of the MR also decreases exocytosis, suggesting that the MR mediates exocytosis. Aldosterone triggers exocytosis within minutes, and this effect is not inhibited by actinomycin D, suggesting a nongenomic effect of aldosterone. Aldosterone treatment of endothelial cells increases leukocyte adherence to endothelial cells in culture. Taken together, our data suggest that aldosterone activates vascular inflammation in part through nongenomic, MR-mediated pathways. Aldosterone antagonism may decrease vascular inflammation and cardiac fibrosis in part by blocking endothelial exocytosis.inflammation ͉ mineralocorticoid ͉ P-selectin ͉ vascular ͉ nitric oxide

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Section: Aldosterone Activates Endothelial Exocytosis Through a Nongementioning

confidence: 52%

mentioning

confidence: 99%

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Aldosterone activates endothelial exocytosis

Jeong¹,

Chaupin²,

Matsushita³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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“…Systemic administration of aldosterone increases oxidative stress in the rat heart, vasculature, and kidney, which activates the redox sensitive NF-B, triggering inflammation [72].…”

Section: Part II -Role Of the Renin-angiotensin-aldosterone System Onmentioning

confidence: 99%

Effects of ACE-Inhibitors and Angiotensin Receptor Blockers on Inflammation

Raimondo¹,

Tuttolomondo²,

Buttà³

et al. 2012

CPD

108

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Abstract:The role of inflammation in cardiovascular disease and in hypertensive disease above all, is complex. Several studies confirm that activation of renin-angiotensin-aldosteron system (RAAS), through increase in the production of angiotensin II (Ang II), is closely related to local vascular inflammation. Over the BP lowering effects of anti-hypertensive treatments, several ancillary effects for every class may be found, distinguishing the various drugs from one another. Given the pro-inflammatory effects of Ang II and aldosterone, agents that interfere with the components of RAAS, such as ACE inhibitors, Angiotensin Recpetor Blockers (ARBs), and mineralocorticoid receptor antagonists (spironolactone or the more selective eplerenone), represent logical therapeutic tools to reduce vascular inflammation and cardiovascular risk, as suggested in large clinical trials in patients with hypertension and diabetes. Regarding ACE inhibitors, actually there is no convincing evidence indicating that ACEi's reduce plasma levels of major inflammatory markers in hypertension models. Lack of evidence concerns especially these inflammation markers, such as fibrinogen of CRP, which are less closely related to atherosclerotic disease and vascular damage and conversely are affected by several more aspecific factors. Results obtained by trials accomplished using ARBs seem to be more univocal to confirm, although to great extent, these is an anti-inflmmatory effect of drugs bocking AT1 receptor. In order to strictly study the effects of blockage of RAAS on inflammation, future studies may explore different strategies by, for example, simultaneously acting on the ACE and the AT1 angiotensin receptors.

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“…Thus, by mineralocorticoid receptor activation, glucocorticoids promote inflammation, oxidative stress, fibrosis, insulin resistance and also endothelial dysfunction. [45][46][47] Moreover, because of insulin resistance, there is decreased insulin stimulation of endothelial NO synthase activation and increased NO destruction. 43 Our results clearly reveal a significant association between RHTN, non-dipping BP and endothelial dysfunction.…”

Section: Nocturnal Dipping and Endothelial Function In Resistant Hypementioning

confidence: 99%

Non-dipping pattern relates to endothelial dysfunction in patients with uncontrolled resistant hypertension

et al. 2011

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Resistant hypertension (RHTN) includes both patients whose blood pressure (BP) is uncontrolled on three or more medications (uncontrolled RHTN (UCRH)) and patients whose BP is controlled with use of four or more drugs (controlled RHTN (CRH)). It is unknown whether endothelial function and nocturnal drop demonstrate a similar pattern in patients with CRH and UCRH. We examined circadian BP patterns and vascular function in these patients. In all, 40 CRH and 26 UCRH patients, and 25 normotensives underwent biochemical testing, ambulatory BP monitoring, determination of brachial artery responses to endothelial-dependent (flow-mediated; dilation (FMD)) and independent (nitroglycerin mediated) stimuli. The nighttime drop in systolic BP (SBP) and diastolic BP (DBP) was less pronounced in UCRH than in CRH (SBP, 1.9±1.6 versus 4.9 ± 1.7%; DBP, 7.5 ± 1.8 versus 10.9 ± 1.8%, UCRH and CRH, respectively; Po0.05). FMD was greater in control group compared with RHTN patients. Patients with UCRH had significantly impaired FMD compared with CRH (5.9 ± 2.3% versus 7.1 ± 5.1%; Po0.0001). Therefore, UCRH patients have less nocturnal dipping and a more impaired endothelial response compared with CRH patients. These findings suggest that important differences among patients with RHTN may allow identify subgroups with increased cardiovascular risk.

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Aldosterone and Vascular Inflammation

Cited by 214 publications

References 105 publications

Aldosterone activates endothelial exocytosis

Aldosterone activates endothelial exocytosis

Effects of ACE-Inhibitors and Angiotensin Receptor Blockers on Inflammation

Non-dipping pattern relates to endothelial dysfunction in patients with uncontrolled resistant hypertension

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