The renin-angiotensin-aldosterone system (RAAS) and cardiac arrhythmias

Iravanian, Shahriar; Dudley, Samuel C.

doi:10.1016/j.hrthm.2008.02.025

Cited by 129 publications

(91 citation statements)

References 79 publications

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“…Recent research has shown that activation of RAAS is important for AF. [33][34][35] RAAS is the key mechanism of atrial remodeling, which is believed to be the main cause of AF. The ACE I/D gene polymorphisms are related to the activity of angiotensin, which is the main effective component of the RAAS.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin-converting enzyme insertion/deletion gene polymorphisms associated with risk of atrial fibrillation: A meta-analysis of 23 case-control studies

et al. 2015

J Renin Angiotensin Aldosterone Syst

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Aims: The renin-angiotensin-aldosterone system is important to the development of atrial fibrillation (AF). A lot of research has focused on the relationship between angiotensin-converting enzyme (ACE) insertion (I) /deletion (D) gene polymorphisms and AF, with inconsistent results. A meta-analysis was carried out to find the correlation between ACE I/D gene polymorphisms and AF. Methods: Data were extracted from articles published before September 2013 on ACE I/D polymorphisms and AF in Embase, PubMed, WanFangData, and China National Knowledge Infrastructure. Results: The recessive model found that ACE I/D gene polymorphisms were related to AF (odds ratio (OR) = 1.61, 95% confidence interval (CI) = 1.16–1.72). Subgroup analysis showed a significant association in the recessive model for Asian (OR = 1.40, 95% CI = 1.19–1.80) and Caucasian (OR = 1.42, 95% CI = 1.01–1.99) populations. Conclusions: ACE I/D gene polymorphisms and AF are significantly related to ethnicity. Individuals with the ACE D/D genotype appear to be at higher risk of AF.

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Section: Discussionmentioning

confidence: 99%

Angiotensin-converting enzyme insertion/deletion gene polymorphisms associated with risk of atrial fibrillation: A meta-analysis of 23 case-control studies

et al. 2015

J Renin Angiotensin Aldosterone Syst

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“…Monitoring the serum levels of the different components of RAAS in heart failure patients has been suggested as a guide to tailor individual therapy (Emdin et al 2015). RAAS activation also seems to be arrhythmogenic, and this goes especially for atrial fibrillation (Iravanian and Dudley 2008). In this case, RAAS activation may lead to alterations in ion channels through increasing oxidative stress.…”

Section: Neurohormonal Signalingmentioning

confidence: 99%

Cardiac aging and heart disease in humans

2017

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The world population continues to grow older rapidly, mostly because of declining fertility and increasing longevity. Since age represents the largest risk factor for cardiovascular disease, the prevalence of these pathologies increases dramatically with increasing age. In order to improve patient care and prevention for age-related cardiac diseases, insight should be gained from the analysis of processes involved in and leading to cardiac aging. It is from this perspective that we provide here an overview of changes associated with age in the heart on four levels: functional, structural, cellular and molecular. We highlight those changes that are in common with the development of the two major age-associated cardiac pathologies: heart failure and atrial fibrillation. These commonly affected processes in aging and cardiac pathophysiology may provide an explanation for the age risk factor in cardiac disease.

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“…Angiotensin II (ANG II), formed locally by mast cell-derived renin in myocardial ischemia (Mackins et al, 2006;Reid et al, 2007), is a major NHE activator via ANG II type 1 receptors (AT 1 Rs) (Reid et al, 2004) and only a minor, indirect inhibitor via AT 2 receptors (Avkiran and Haworth, 2003). ANG II elicits reperfusion arrhythmias by a direct action (Harada et al, 1998;Yahiro et al, 2003;Iravanian and Dudley, 2008), as well as by facilitating NE release (Schömig, 1990;Meredith et al, 1991;Levi and Smith, 2000); both of these actions are AT 1 Rmediated .…”

Section: Introductionmentioning

confidence: 99%

Histamine 3 Receptor Activation Reduces the Expression of Neuronal Angiotensin II Type 1 Receptors in the Heart

Hashikawa-Hobara¹,

Chan²,

Levi³

2011

J Pharmacol Exp Ther

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In severe myocardial ischemia, histamine 3 (H 3 ) receptor activation affords cardioprotection by preventing excessive norepinephrine release and arrhythmias; pivotal to this action is the inhibition of neuronal Na ϩ /H ϩ exchanger (NHE). Conversely, angiotensin II, formed locally by mast cell-derived renin, stimulates NHE via angiotensin II type 1 (AT 1 ) receptors, facilitating norepinephrine release and arrhythmias. Thus, ischemic dysfunction may depend on a balance between the NHE-modulating effects of H 3 receptors and AT 1 receptors. The purpose of this investigation was therefore to elucidate the H 3 /AT 1 receptor interaction in myocardial ischemia/reperfusion. We found that H 3 receptor blockade with clobenpropit increased norepinephrine overflow and arrhythmias in Langendorff-perfused guinea pig hearts subjected to ischemia/reperfusion. This coincided with increased neuronal AT 1 receptor expression. NHE inhibition with cariporide prevented both increases in norepinephrine release and AT 1 receptor expression. Moreover, norepinephrine release and AT 1 receptor expression were increased by the nitric oxide (NO) synthase inhibitor N G -methyl-L-arginine and the protein kinase C activator phorbol myristate acetate. H 3 receptor activation in differentiated sympathetic neuron-like PC12 cells permanently transfected with H 3 receptor cDNA caused a decrease in protein kinase C activity and AT 1 receptor protein abundance. Collectively, our findings suggest that neuronal H 3 receptor activation inhibits NHE by diminishing protein kinase C activity. Reduced NHE activity sequentially causes intracellular acidification, increased NO synthesis, and diminished AT 1 receptor expression. Thus, H 3 receptor-mediated NHE inhibition in ischemia/reperfusion not only opposes the angiotensin II-induced stimulation of NHE in cardiac sympathetic neurons, but also down-regulates AT 1 receptor expression. Cardioprotection ultimately results from the combined attenuation of angiotensin II and norepinephrine effects and alleviation of arrhythmias.

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The renin-angiotensin-aldosterone system (RAAS) and cardiac arrhythmias

Cited by 129 publications

References 79 publications

Angiotensin-converting enzyme insertion/deletion gene polymorphisms associated with risk of atrial fibrillation: A meta-analysis of 23 case-control studies

Angiotensin-converting enzyme insertion/deletion gene polymorphisms associated with risk of atrial fibrillation: A meta-analysis of 23 case-control studies

Cardiac aging and heart disease in humans

Histamine 3 Receptor Activation Reduces the Expression of Neuronal Angiotensin II Type 1 Receptors in the Heart

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