Development of neuropeptide Y-mediated heart innervation in rats

Maslyukov, P. M.; Moiseev, K. Yu.; Emanuilov, A. I.; Anikina, T. A.; Zverev, A. A.; Nozdrachev, A. D.

doi:10.1016/j.npep.2015.10.007

Cited by 15 publications

(4 citation statements)

References 46 publications

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“…The majority of NPY immunoreactive fibers are post-ganglionic, originating from the SG and colocalizing with tyrosine hydroxylase ( Masliukov et al, 2016 ). Sympathetic nerve terminals, which can act as local neuromodulators in various cardiovascular disorders, represent one of the main sources of NPY ( Tan et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

Upregulation of neuropeptide Y in cardiac sympathetic nerves induces stress (Takotsubo) cardiomyopathy

Arai

Kimura²,

Munakata

et al. 2022

Front. Neurosci.

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Substantial emotional or physical stress may lead to an imbalance in the brain, resulting in stress cardiomyopathy (SC) and transient left ventricular (LV) apical ballooning. Even though these conditions are severe, their precise underlying mechanisms remain unclear. Appropriate animal models are needed to elucidate the precise mechanisms. In this study, we established a new animal model of epilepsy-induced SC. The SC model showed an increased expression of the acute phase reaction protein, c-Fos, in the paraventricular hypothalamic nucleus (PVN), which is the sympathetic nerve center of the brain. Furthermore, we observed a significant upregulation of neuropeptide Y (NPY) expression in the left stellate ganglion (SG) and cardiac sympathetic nerves. NPY showed neither positive nor negative inotropic and chronotropic effects. On the contrary, NPY could interrupt β-adrenergic signaling in cardiomyocytes when exposure to NPY precedes exposure to noradrenaline. Moreover, its elimination in the left SG via siRNA treatment tended to reduce the incidence of SC. Thus, our results indicated that upstream sympathetic activation induced significant upregulation of NPY in the left SG and cardiac sympathetic nerves, resulting in cardiac dysfunctions like SC.

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Section: Discussionmentioning

confidence: 99%

Upregulation of neuropeptide Y in cardiac sympathetic nerves induces stress (Takotsubo) cardiomyopathy

Arai

Kimura²,

Munakata

et al. 2022

Front. Neurosci.

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“…Moreover, NPY is known as a substance that reduces acetylcholine release [47] and therefore attenuates vagal bradycardia [48], as well as shows pro-arrhythmic activity by direct impact on the ventricular electrophysiology [49]. Apart from the influence on cardiomyocyte contraction, NPY is known as an important trophic factor taking part in heart development [50] and a substance that influences blood vessels and improves myocardial perfusion [51]. This neuropeptide also participates in the development of some heart and cardiovascular diseases, including hypertension, myocardial infarction and chronic heart failure [52].…”

Section: Discussionmentioning

confidence: 99%

Changes Caused by Low Doses of Bisphenol A (BPA) in the Neuro-Chemistry of Nerves Located in the Porcine Heart

Makowska

Gonkowski

2021

Animals

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Bisphenol A (BPA) contained in plastics used in the production of various everyday objects may leach from these items and contaminate food, water and air. As an endocrine disruptor, BPA negatively affects many internal organs and systems. Exposure to BPA also contributes to heart and cardiovascular system dysfunction, but many aspects connected with this activity remain unknown. Therefore, this study aimed to investigate the impact of BPA in a dose of 0.05 mg/kg body weight/day (in many countries such a dose is regarded as a tolerable daily intake–TDI dose of BPA–completely safe for living organisms) on the neurochemical characterization of nerves located in the heart wall using the immunofluorescence technique. The obtained results indicate that BPA (even in such a relatively low dose) increases the number of nerves immunoreactive to neuropeptide Y, substance P and tyrosine hydroxylase (used here as a marker of sympathetic innervation). However, BPA did not change the number of nerves immunoreactive to vesicular acetylcholine transporter (used here as a marker of cholinergic structures). These observations suggest that changes in the heart innervation may be at the root of BPA-induced circulatory disturbances, as well as arrhythmogenic and/or proinflammatory effects of this endocrine disruptor. Moreover, changes in the neurochemical characterization of nerves in the heart wall may be the first sign of exposure to BPA.

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“…The ECG changes observed following cerebral ischemia may be mediated through abnormal autonomic discharges caused by increased levels of brain natriuretic peptide, catecholamines, and NPY [21, 35, 36]. NPY released by sympathetic neurons can reduce vagal neurotransmission and directly influence ventricular myocyte excitability.…”

Section: Interaction Between Cardiovascular Changes and Specific Bmentioning

confidence: 99%

“…NPY is widely distributed in both the central and peripheral nervous systems and is functionally related to regulation of blood pressure and circadian rhythms. Further, as a potent growth factor, NPY can cause cell proliferation in multiple systems, especially in the cardiovascular system [36], which is associated with cardiac hypertrophy via increased protein synthesis [39] and innervation-dependent changes in catecholamine-dependent chronotropic responsiveness [40]. Finally, there is increasing evidence that neurons can release NPY after myocardial infarction, which is involved in the progress of bilateral interventions targeting the sympathetic chain for arrhythmia modulation [24, 25, 41].…”

Section: Interaction Between Cardiovascular Changes and Specific Bmentioning

confidence: 99%

Neurocardiology: Cardiovascular Changes and Specific Brain Region Infarcts

Zou

Shi

Tao

et al. 2017

BioMed Research International

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There are complex and dynamic reflex control networks between the heart and the brain, including cardiac and intrathoracic ganglia, spinal cord, brainstem, and central nucleus. Recent literature based on animal model and clinical trials indicates a close link between cardiac function and nervous systems. It is noteworthy that the autonomic nervous-based therapeutics has shown great potential in the management of atrial fibrillation, ventricular arrhythmia, and myocardial remodeling. However, the potential mechanisms of postoperative brain injury and cardiovascular changes, particularly heart rate variability and the presence of arrhythmias, are not understood. In this chapter, we will describe mechanisms of brain damage undergoing cardiac surgery and focus on the interaction between cardiovascular changes and damage to specific brain regions.

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Development of neuropeptide Y-mediated heart innervation in rats

Cited by 15 publications

References 46 publications

Upregulation of neuropeptide Y in cardiac sympathetic nerves induces stress (Takotsubo) cardiomyopathy

Upregulation of neuropeptide Y in cardiac sympathetic nerves induces stress (Takotsubo) cardiomyopathy

Changes Caused by Low Doses of Bisphenol A (BPA) in the Neuro-Chemistry of Nerves Located in the Porcine Heart

Neurocardiology: Cardiovascular Changes and Specific Brain Region Infarcts

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