Parasympathetic and substance P-immunoreactive nerve denervation in atrial fibrillation models

Yu, Ying; Liu, Li; Jiang, Jiuyang; Qu, Xiu Fen; Yu, Guang

doi:10.1016/j.carpath.2011.01.003

Cited by 8 publications

(9 citation statements)

References 23 publications

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“…Sub-P is widely distributed in the cardiovascular system and is involved in the regulation of many physiological functions, including heart rate (through stimulation of cholinergic neurons) and blood pressure 17 , 18 . Reduced Sub-P content has been associated with AF incidence 19 , 20 . Specifically, the occurrence of post-operational AF was associated with decreased Sub-P serum levels in patients who had undergone coronary artery bypass surgery 19 .…”

Section: Introductionmentioning

confidence: 99%

Neurokinin-3 receptor activation selectively prolongs atrial refractoriness by inhibition of a background K+ channel

Veldkamp

Geuzebroek²,

Baartscheer

et al. 2018

Nat Commun

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The cardiac autonomic nervous system (ANS) controls normal atrial electrical function. The cardiac ANS produces various neuropeptides, among which the neurokinins, whose actions on atrial electrophysiology are largely unknown. We here demonstrate that the neurokinin substance-P (Sub-P) activates a neurokinin-3 receptor (NK-3R) in rabbit, prolonging action potential (AP) duration through inhibition of a background potassium current. In contrast, ventricular AP duration was unaffected by NK-3R activation. NK-3R stimulation lengthened atrial repolarization in intact rabbit hearts and consequently suppressed arrhythmia duration and occurrence in a rabbit isolated heart model of atrial fibrillation (AF). In human atrial appendages, the phenomenon of NK-3R mediated lengthening of atrial repolarization was also observed. Our findings thus uncover a pathway to selectively modulate atrial AP duration by activation of a hitherto unidentified neurokinin-3 receptor in the membrane of atrial myocytes. NK-3R stimulation may therefore represent an anti-arrhythmic concept to suppress re-entry-based atrial tachyarrhythmias, including AF.

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Section: Introductionmentioning

confidence: 99%

Neurokinin-3 receptor activation selectively prolongs atrial refractoriness by inhibition of a background K+ channel

Veldkamp

Geuzebroek²,

Baartscheer

et al. 2018

Nat Commun

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“…Autonomic remodeling was characterized by increased sympathetic innervation of the atria as well as increased heterogeneity of atrial sympathetic innervation. In the succeeding study, we found denervation of parasympathetic nerves in the atria . Not only sympathetic and vagal nerve involved in neural remodeling, some neuropeptides also changed during AF.…”

Section: Discussionmentioning

confidence: 56%

“…Neuropeptide Y, a sympathetic neurotransmitter increased in the atria by pacing induced AF . While vasoactive intestinal peptide, a parasympathetic cotransmitter and substance P a marker of afferent nerve decreased significantly . The nerve terminals in the atria derive from extrinsic and intrinsic origins.…”

Section: Discussionmentioning

confidence: 82%

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Atrial Fibrillation Increases Sympathetic and Parasympathetic Neurons in the Intrinsic Cardiac Nervous System

Wei

Liu

et al. 2014

Pacing Clinical Electrophis

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“…A loss of cardiac SP may also predispose the heart to atrial fibrillation. Yu et al, [49] paced dog hearts (600 beats/minute) to induce atrial fibrillation and found that although there was an increase in sympathetic nerve fibers in the atria, there was a dramatic loss of SP-containing nerve fibers. Guler et al, [50] reported that plasma levels of SP significantly decreased in patients two days after coronary artery bypass surgery.…”

Section: 0 Substance P (Sp)mentioning

confidence: 99%

The role of neuropeptides in adverse myocardial remodeling and heart failure

Widiapradja

Chunduri

Levick

2017

Cell. Mol. Life Sci.

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In addition to traditional neurotransmitters of the sympathetic and parasympathetic nervous systems, the heart also contains numerous neuropeptides. These neuropeptides not only modulate the effects of neurotransmitters, but also have independent effects on cardiac function. While in most cases the physiological actions of these neuropeptides are well defined, their contributions to cardiac pathology are less appreciated. Some neuropeptides are cardioprotective, some promote adverse cardiac remodeling and heart failure, and in the case of others their functions are unclear. Some have both cardioprotective and adverse effects depending on the specific cardiac pathology and progression of that pathology. In this review, we briefly describe the actions of several neuropeptides on normal cardiac physiology, before describing in more detail their role in adverse cardiac remodeling and heart failure. It is our goal to bring more focus toward understanding the contribution of neuropeptides to the pathogenesis of heart failure, and to consider them as potential therapeutic targets.

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Parasympathetic and substance P-immunoreactive nerve denervation in atrial fibrillation models

Cited by 8 publications

References 23 publications

Neurokinin-3 receptor activation selectively prolongs atrial refractoriness by inhibition of a background K+ channel

Neurokinin-3 receptor activation selectively prolongs atrial refractoriness by inhibition of a background K+ channel

Atrial Fibrillation Increases Sympathetic and Parasympathetic Neurons in the Intrinsic Cardiac Nervous System

The role of neuropeptides in adverse myocardial remodeling and heart failure

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