Relationship of myocardial remodeling to the genesis of serum autoantibodies to cardiac beta1-adrenoceptors and muscarinic type 2 acetylcholine receptors in rats

Liu, Hui Rong; Zhao, Rong; Jiao, Xiang; Wang, Ying Yuan; Fu, Michael

doi:10.1016/s0735-1097(02)01865-x

Cited by 56 publications

(44 citation statements)

References 16 publications

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“…5,[21][22][23][24][25] In an animal model, autoantibodies have been associated with remodeling in HF, but it is not certain how the two are related. 26 M 2 receptor predominance also was observed to shift to M 3 and M 4 receptors. Cardiac M 3 receptors may affect heart rate and cardiac repolarization, modulate inotropic effects, protect against ischemic injury, regulate cell-cell communication, and have antiarrhythmic and proarrhythmic effects.…”

Section: Muscarinic Receptorsmentioning

confidence: 78%

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Parasympathetic Nervous System and Heart Failure

et al. 2008

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A bundant evidence links sympathetic nervous system activation to outcomes of patients with heart failure (HF). 1 In contrast, parasympathetic activation has complex cardiovascular effects that are only beginning to be recognized. In particular, the pathophysiological roles of normal and disordered parasympathetic innervation in patients with HF are not understood as comprehensively. [2][3][4][5] In the present article, we review cardiovascular responses to parasympathetic activation, address the modulating factors that can affect parasympathetic function, discuss the role of the vagus nerve in ventricular dysfunction, and consider how activation of the parasympathetic nervous system may have important therapeutic implications for patients with congestive HF. Structure of the Parasympathetic Limb of the Autonomic Nervous SystemThe parasympathetic nervous system originates from medial medullary sites (nucleus ambiguous, nucleus tractus solitarius, and dorsal motor nucleus) and is modulated by the hypothalamus. Vagal efferents extend from the medulla to postganglionic nerves that innervate the atria via ganglia located in cardiac fat pads with neurotransmission that is modulated via nicotinic receptors. Postganglionic parasympathetic and sympathetic cholinergic nerves then affect cardiac muscarinic receptors (the Figure). 6 -8 Vagus nerve afferent activation, originating peripherally, can modulate efferent sympathetic and parasympathetic function centrally and at the level of the baroreceptor.Efferent vagus nerve activation can have tonic and basal effects that inhibit sympathetic activation and release of norepinephrine at the presynaptic level. Acetylcholine release from parasympathetic nerve terminals will activate ganglionic nicotinic receptors that in turn activate muscarinic receptors at the cellular level. Cardiovascular effects include heart rate reduction by inhibition of the sympathetic nervous system and by direct hyperpolarization of sinus nodal cells. Parasympathetic activation can affect atrioventricular nodal conduction mediated predominantly through the left vagus nerve. Furthermore, muscarinic receptors on blood vessel walls can cause vasorelaxation through a nitric oxide (NO)-modulated pathway but can also cause vasoconstriction by directly activating smooth muscle. 6 -8 Therefore, although the sympathetic nervous system has global effects on cardiovascular physiology in an all-or-none type of response, the parasympathetic nervous system can have selective modulation at various levels. Parasympathetic/Sympathetic InteractionsThe sympathetic and parasympathetic nervous systems are not "opposites"; rather, the interactions are complex. 9 A dynamic interaction occurs between them; these interactions are modulated partially by secondary messengers (cAMP and cGMP). The parasympathetic nervous system can inhibit sympathetic nerve traffic presynaptically. Likewise, sympathetic activation can inhibit parasympathetic activation presynaptically.Vagal "tone" (tonic parasympathetic activation) predominates...

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Section: Muscarinic Receptorsmentioning

confidence: 78%

“…Additionally, M 2 receptors on the presynaptic sympathetic nerve terminal will inhibit norepinephrine release. [21][22][23]26 Heart Rate and Outcomes…”

Section: Heart Rate Controlmentioning

confidence: 99%

Parasympathetic Nervous System and Heart Failure

et al. 2008

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“…The circulating levels of ␤1-AR autoantibodies were markedly increased by induction of experimental heart failure and cardiomyopathy in animal models. 35 In recent years, blocking ␤1-AR with specific antagonists has been refined as a potential therapeutic strategy to effectively modulate the stimulating and uncoupling effects of ␤1-AR autoantibodies. Although several studies show an improved outcome of ␤-blockers in a clinical setting, more specific agents directed against the activating site of the autoantibodies are under development.…”

Section: Non-standard Abbreviations and Acronymsmentioning

confidence: 99%

Autoantibodies in Heart Failure and Cardiac Dysfunction

Kaya

Leib

Katus

2012

Circulation Research

165

151

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Abstract:Human heart failure is a disease with multifactorial causes, considerable morbidity, and high mortality.Several circulating autoantibodies, some of them being heart-specific, play a crucial role in the progression and induction of heart failure. However the precise mechanisms on how these autoantibodies perpetuate or even induce an organ specific autoimmune response are not yet fully understood. Also it is being a matter of current research to elucidate a potential pathophysiological role of the innate immune system in generating auto-reactive antibodies. In this review we will summarize the current available literature on circulating autoantibodies which are related to human heart failure. We will present clinical and animal studies that demonstrate the occurrence and pathophysiological relevance of several autoantibodies in heart failure, as well as point out biological mechanisms on molecular and cellular level. Finally the beneficial therapeutic effects of numerous clinical studies that target the humoral arm of the immune system by using either intravenous immunoglobulins and/or immunoadsorption will be critically discussed. (Circ Res. 2012;110:145-158.)

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“…There are many types of receptors such as dopamine receptors [1,2,3], acetylcholine receptors [4][5][6], serotonin and 5HT2A receptors [1,7], adrenergic receptors [8][9][10][11], estrogen receptors [12,13], and steroid receptors [14] Basically, one approach to the development of a new radioiodinated myocardial agent is the radioiodination of drug analogues that exert cardio selective pharmacological action (i.e. competitive adrenoceptors blockade drugs).…”

Section: Introductionmentioning

confidence: 99%

Preparation of Labelled dopamine by 125I using Lactoperoxidase and N- Bromosuccinamide

El-Mouhty¹,

Shehab

2012

International Journal of Basic and Applied Sciences

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The present study was carried out to prepare 125 I-dopamine Tracer, using oxidizing agents such as Lactoperoxidase and NBromosuccinamide , which was purified by column sephadex G-75 and used to study the biodistribution in normal Albino Swiss mice and the results indicate the possibility of using [125 I] iodo dopamine as myocardial imaging agent. The conditions of radioiodination such as concentration of oxidizing agent, reaction time, concentration of Atenolol and effect of pH were studied to get maximum yield. Stability study of dopamine tracer was carried out.

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Relationship of myocardial remodeling to the genesis of serum autoantibodies to cardiac beta1-adrenoceptors and muscarinic type 2 acetylcholine receptors in rats

Abstract: Our results demonstrated that myocardial damage was able to trigger the occurrence of an autoimmune reaction, resulting in the genesis of anticardiac receptor autoantibodies with properties similar to those seen in patients with idiopathic dilated cardiomyopathy.

Cited by 56 publications

References 16 publications

Parasympathetic Nervous System and Heart Failure

Parasympathetic Nervous System and Heart Failure

Autoantibodies in Heart Failure and Cardiac Dysfunction

Preparation of Labelled dopamine by 125I using Lactoperoxidase and N- Bromosuccinamide

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