Atrial Natriuretic Peptide Has Dose‐Dependent, Autonomically Mediated Effects on Atrial Refractoriness and Repolarization in Anesthetized Dogs

Stambler, Bruce S.; Guo, G. Bih-Fang

doi:10.1111/j.1540-8167.2005.00259.x

Cited by 17 publications

(3 citation statements)

References 36 publications

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“…The anti-inflammatory effect of RSD treatment may have relationship with the suppressed plasma levels of Ang II and aldosterone. ANP is released in response to atrial stretch, and studies suggested that ANP has dose-dependent, autonomically mediated effects on atrial refractoriness and repolarization and plays a role in atrial fibrosis of AF [31], [32]. In addition, Our present study suggests that RSD treatment could attenuate the increase in left atrial level of ANP that is induced by CRAP and could markedly alleviate the lesion degree of cardic fibrosis compared with the CRAP group, thus suppressing atrial remodeling.…”

Section: Discussionsupporting

confidence: 57%

Effect of Renal Sympathetic Denervation on Atrial Substrate Remodeling in Ambulatory Canines with Prolonged Atrial Pacing

et al. 2013

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We have previously demonstrated that catheter-based renal sympathetic denervation (RSD) could suppress atrial fibrillation (AF) in canines with short-time rapid right atrial pacing (RAP). However, the role of renal denervation on atrial remodeling is unclear. The aim of the present study was to explore the long-term effect of RSD on the atrial remodeling during prolonged RAP. Twenty mongrel dogs were implanted with a high-frequency cardiac pacemaker with a transvenous lead inserted into the right atrial appendage. The dogs were divided into three groups: a sham-operated group (n = 6), the chronic RAP (CRAP) group (n = 7), and the CRAP+RSD group (n = 7). In the CRAP+RSD group, a pacemaker was implanted 6 weeks after RSD was performed bilaterally for recovery. RAP was maintained for 5 weeks in CRAP group and CRAP+RSD group. The plasma levels of Angiotensin II and aldosterone were significantly increased in CRAP group compared with sham-operated group, but the increasing trend was inhibited in CRAP+RSD group compared with CRAP group (P<0.05). Similarly, RSD suppressed the increasing trend that prolonged RAP produced in the left atrial levels of ANP, TNF-α and IL-6. Compared with the sham-operated group, the CRAP group had significantly increased levels of caspase-3, bax and Cx40 whereas the level of Bcl-2 decreased (P<0.05). RSD markedly reduced the upregulation of caspase-3, bax and Cx40 and the downregulation of Bcl-2 expression compared with the CRAP group (P<0.05). Picric acid–sirius red staining study suggested that RSD could markedly alleviate the lesion degree of cardic fibrosis induced by CRAP (P<0.05). Immunohistochemistry results showed that the densities of TH- and GAP43- positive nerves were significantly elevated in the CRAP group compared with the sham-operated group, while RSD operation signicantly inhibited the these changes produced by CRAP. These findings suggest that renal denervation could suppress the atrial remodeling after prolonged RAP in ambulatory canines.

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Section: Discussionsupporting

confidence: 57%

Effect of Renal Sympathetic Denervation on Atrial Substrate Remodeling in Ambulatory Canines with Prolonged Atrial Pacing

et al. 2013

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“…Natriuretic peptide A-codifying gene has also been found mutated in AF, by altering the physiologic control exerted by this circulating hormone in the modulation of the neurohormonal stimulation and of ion channels [262][263][264][265]. A two-base-pair deletion was identified in the NPPA gene by Hodgson-Zingman and colleagues employing genomewide association study and pyrosequencing.…”

Section: Modeling Of Af-related Nppa Mutationsmentioning

confidence: 99%

Inherited and Acquired Rhythm Disturbances in Sick Sinus Syndrome, Brugada Syndrome, and Atrial Fibrillation: Lessons from Preclinical Modeling

Iop

Iliceto

Civieri

et al. 2021

Cells

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Rhythm disturbances are life-threatening cardiovascular diseases, accounting for many deaths annually worldwide. Abnormal electrical activity might arise in a structurally normal heart in response to specific triggers or as a consequence of cardiac tissue alterations, in both cases with catastrophic consequences on heart global functioning. Preclinical modeling by recapitulating human pathophysiology of rhythm disturbances is fundamental to increase the comprehension of these diseases and propose effective strategies for their prevention, diagnosis, and clinical management. In silico, in vivo, and in vitro models found variable application to dissect many congenital and acquired rhythm disturbances. In the copious list of rhythm disturbances, diseases of the conduction system, as sick sinus syndrome, Brugada syndrome, and atrial fibrillation, have found extensive preclinical modeling. In addition, the electrical remodeling as a result of other cardiovascular diseases has also been investigated in models of hypertrophic cardiomyopathy, cardiac fibrosis, as well as arrhythmias induced by other non-cardiac pathologies, stress, and drug cardiotoxicity. This review aims to offer a critical overview on the effective ability of in silico bioinformatic tools, in vivo animal studies, in vitro models to provide insights on human heart rhythm pathophysiology in case of sick sinus syndrome, Brugada syndrome, and atrial fibrillation and advance their safe and successful translation into the cardiology arena.

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“…In addition cardiac ion channels (sodium, potassium and calcium) are regulated by ANP through cGMP signaling 34,35,36 . ANP can promote AF either by shortening of the atrial action potential duration (APD) and effective refractory period (ERP), 37 or by autonomically-mediated shortening of the atrial monophasic action potential (MAP) duration and the ERP in dogs 38 . Therefore, it is hypothesized that NPPA mutation can lead to AF.…”

Section: Cardiac Developmental Pathwaysmentioning

confidence: 99%

Improved understanding of the pathophysiology of atrial fibrillation through the lens of discrete pathological pathways

Balouch

Kolek

Darbar

2014

Global Cardiology Science and Practice

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Atrial fibrillation (AF) is a common disorder with a complex and incompletely understood pathophysiology. Genetic approaches to understanding the pathophysiology of AF have led to the identification of several biological pathways important in the pathogenesis of the arrhythmia. These include pathways important for cardiac development, generation and propagation of atrial electrical impulses, and atrial remodeling and fibrosis. While common and rare genetic variants in these pathways are associated with increased susceptibility to AF, they differ substantially among patients with lone versus typical AF. Furthermore, how these pathways converge to a final common clinical phenotype of AF is unclear and might also vary among different patient populations. Here, we review the contemporary knowledge of AF pathogenesis and discuss how derangement in cardiac development, ion channel dysfunction, and promotion of atrial fibrosis may contribute to this common and important clinical disorder.

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Atrial Natriuretic Peptide Has Dose‐Dependent, Autonomically Mediated Effects on Atrial Refractoriness and Repolarization in Anesthetized Dogs

Abstract: ANP has dose-dependent, autonomically mediated effects on atrial refractoriness and repolarization.

Cited by 17 publications

References 36 publications

Effect of Renal Sympathetic Denervation on Atrial Substrate Remodeling in Ambulatory Canines with Prolonged Atrial Pacing

Effect of Renal Sympathetic Denervation on Atrial Substrate Remodeling in Ambulatory Canines with Prolonged Atrial Pacing

Inherited and Acquired Rhythm Disturbances in Sick Sinus Syndrome, Brugada Syndrome, and Atrial Fibrillation: Lessons from Preclinical Modeling

Improved understanding of the pathophysiology of atrial fibrillation through the lens of discrete pathological pathways

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