scholarly journals The Brain-Heart Connection in Takotsubo Syndrome: The Central Nervous System, Sympathetic Nervous System, and Catecholamine Overload

2020 ◽  
Vol 2020 ◽  
pp. 1-5 ◽  
Author(s):  
Xiaopu Wang ◽  
Junyu Pei ◽  
Xinqun Hu
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Physiological Stress ◽  
Acute Chest Pain ◽  
Takotsubo Syndrome ◽  
The Central Nervous System ◽  
Sympathetic Nervous ◽  
As Stress ◽  
Artery Obstruction ◽  
The Brain

Takotsubo syndrome (TTS), also known as stress cardiomyopathy, is a type of acute heart failure syndrome triggered by intense psychological or physiological stress. TTS typically manifests as acute chest pain, dyspnea or syncope that mimics an acute myocardial infarction but does not involve coronary artery obstruction. The current understanding of the pathogenesis of TTS suggests that sympathetic nervous system (SNS) activation plays a central role. Specifically, stress can activate the SNS and lead to the over-release of catecholamine, which have toxic effects on myocardial tissue when present at excessive levels. However, the brain changes associated with TTS and the connection between the brain and the heart in patients with this disease remain unclear. In recent years, several published reports have revealed the role of this brain-heart connection in the pathogenesis of TTS. This review summarizes recent studies regarding SNS activation, catecholamine overload, and the brain-heart connection in patients with TTS from both pathophysiological and mechanistic aspects.

scholarly journals Takotsubo Syndrome: A Review on The Relationship Between The Heart and The Brain

2021 ◽  
Author(s):  
Prima Hapsari Wulandari
Keyword(s):  
Nervous System ◽  
Acute Chest Pain ◽  
Scientific Data ◽  
Stress Cardiomyopathy ◽  
Takotsubo Syndrome ◽  
The Central Nervous System ◽  
As Stress ◽  
Artery Obstruction ◽  
The Relationship ◽  
The Brain

Takotsubo syndrome (TTS), also known as stress cardiomyopathy, causes severe heart syndrome in humans due to extreme physiological and psychological stress events in life. Takotsubo syndrome's critical manifestations of acute chest pain and syncope or dyspnea often imitate an episode of severe myocardial infarction that does not entail coronary artery obstruction. Recent scientific data reveals that the sympathetic nervous system (SNS) stimulation contributes significantly to the pathogenesis of TTS. In detail, emotional stress events in an individual cause SNS activation, leading to an excessive release of catecholamine that inflicts toxicity to myocardial tissues when present at superfluous concentrations. However, the central nervous system (CNS) alterations and the relationship between heart and brain among TTS patients remain vague. Of late, several published studies disclosed the importance of the aforesaid heart-brain relationship in the pathogenesis of TTS. This review examines studies focused on the excessive release of catecholamine, the activation of SNS, and the heart-brain relationship in TTS cases from concurrent systemic and pathophysiological attributes.

scholarly journals Dr. A. I. Yushchenko. The relationship of the lower mesenteric sympathetic node to the innervation of the bladder and the volume of automatic movements of the last day. - Archive of Biological Sciences, T. VI, issue 5

2020 ◽  
Vol VI (4) ◽  
pp. 213-214
Author(s):  
B. I. Vorotynskiy
Keyword(s):  
Biological Sciences ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Morphological Properties ◽  
The Central Nervous System ◽  
Sympathetic Nervous ◽  
The Right ◽  
Relationship Of ◽  
The Relationship ◽  
The Brain

Physiology has not yet given us positive data on the function of the sympathetic nervous system. Only recently, histologists have been able to prove that the nerve cells located in large sympathetic nodes do not differ in their morphological properties from cells of the central nervous system. This gives the right to assume that in the sympathetic nodes there are independent centers that are in the same dependence on the higher centers, as, for example, the centers of the spinal cord from the brain. We have very little data on the relationship of the sympathetic nervous system to the innervations of the bladder. On this basis, the author began to study this issue in the physiological laboratory of prof. Pavlova at the M. Academy.

The Role of Noradrenaline and other Transmitter Hormones in the Pathogenesis of Hypertension

1976 ◽  
Vol 51 (s3) ◽  
pp. 427s-430s
Author(s):  
W. J. Louis ◽  
B. Jarrott ◽  
A. E. Doyle
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Essential Hypertension ◽  
Sympathetic Nervous System ◽  
Radioenzymatic Assay ◽  
The Central Nervous System ◽  
Serotonin Turnover ◽  
Mesenteric Vessels ◽  
Sympathetic Nervous

1. Studies with a sensitive radioenzymatic assay for plasma noradrenaline suggest there is a selective overactivity of the sympathetic nervous system in essential hypertension. 2. Serotonin turnover in the mesenteric vessels is approximately twice that of noradrenaline and it is suggested that serotonin may interact with noradrenaline to maintain vascular resistance. 3. Methodology which allows the study of local sympathetic turnover in nuclei of the central nervous system and in peripheral blood vessels is described. This approach has been used to study non-innervated sympathetic turnover observed in phaeochromocytoma.

scholarly journals Central Fibroblast Growth Factor 21 Browns White Fat via Sympathetic Action in Male Mice

Endocrinology ◽  
2015 ◽  
Vol 156 (7) ◽  
pp. 2470-2481 ◽  
Author(s):  
Nicholas Douris ◽  
Darko M. Stevanovic ◽  
ffolliott M. Fisher ◽  
Theodore I. Cisu ◽  
Melissa J. Chee ◽  
...  
Keyword(s):  
Nervous System ◽  
Adipose Tissue ◽  
Growth Factor ◽  
Sympathetic Nervous System ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 21 ◽  
Fibroblast Growth ◽  
Male Mice ◽  
Sympathetic Nervous ◽  
The Brain

Fibroblast growth factor 21 (FGF21) has multiple metabolic actions, including the induction of browning in white adipose tissue. Although FGF21 stimulated browning results from a direct interaction between FGF21 and the adipocyte, browning is typically associated with activation of the sympathetic nervous system through cold exposure. We tested the hypothesis that FGF21 can act via the brain, to increase sympathetic activity and induce browning, independent of cell-autonomous actions. We administered FGF21 into the central nervous system via lateral ventricle infusion into male mice and found that the central treatment increased norepinephrine turnover in target tissues that include the inguinal white adipose tissue and brown adipose tissue. Central FGF21 stimulated browning as assessed by histology, expression of uncoupling protein 1, and the induction of gene expression associated with browning. These effects were markedly attenuated when mice were treated with a β-blocker. Additionally, neither centrally nor peripherally administered FGF21 initiated browning in mice lacking β-adrenoceptors, demonstrating that an intact adrenergic system is necessary for FGF21 action. These data indicate that FGF21 can signal in the brain to activate the sympathetic nervous system and induce adipose tissue thermogenesis.

Imbalance of central nitric oxide and reactive oxygen species in the regulation of sympathetic activity and neural mechanisms of hypertension

2011 ◽  
Vol 300 (4) ◽  
pp. R818-R826 ◽  
Author(s):  
Yoshitaka Hirooka ◽  
Takuya Kishi ◽  
Koji Sakai ◽  
Akira Takeshita ◽  
Kenji Sunagawa
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Brain Stem ◽  
Intracellular Signaling ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Sympathetic Nervous ◽  
The Brain

Nitric oxide (NO) and reactive oxygen species (ROS) play important roles in blood pressure regulation via the modulation of the autonomic nervous system, particularly in the central nervous system (CNS). In general, accumulating evidence suggests that NO inhibits, but ROS activates, the sympathetic nervous system. NO and ROS, however, interact with each other. Our consecutive studies and those of others strongly indicate that an imbalance between NO bioavailability and ROS generation in the CNS, including the brain stem, activates the sympathetic nervous system, and this mechanism is involved in the pathogenesis of neurogenic aspects of hypertension. In this review, we focus on the role of NO and ROS in the regulation of the sympathetic nervous system within the brain stem and subsequent cardiovascular control. Multiple mechanisms are proposed, including modulation of neurotransmitter release, inhibition of receptors, and alterations of intracellular signaling pathways. Together, the evidence indicates that an imbalance of NO and ROS in the CNS plays a pivotal role in the pathogenesis of hypertension.

scholarly journals Pathophysiology of Takotsubo Syndrome as A Bridge to Personalized Treatment

2021 ◽  
Vol 11 (9) ◽  
pp. 879
Author(s):  
Monika Budnik ◽  
Radosław Piątkowski ◽  
Dorota Ochijewicz ◽  
Martyna Zaleska ◽  
Marcin Grabowski ◽  
...  
Keyword(s):  
Nervous System ◽  
Genetic Factors ◽  
Personalized Treatment ◽  
Takotsubo Syndrome ◽  
Primary Condition ◽  
Psychiatric Conditions ◽  
Sympathetic Nervous ◽  
Vessel Dissection ◽  
The Brain ◽  
Microcirculation Dysfunction

Takotsubo syndrome (TTS) consists of transient dysfunction of the left and/or right ventricle in the absence of ruptured plaque; thrombus or vessel dissection. TTS may be divided into two categories. Primary TTS occurs when the cause of hospitalization is the symptoms resulting from damage to the myocardium usually preceded by emotional stress. Secondary TTS occurs in patients hospitalized for other medical; surgical; anesthetic; obstetric or psychiatric conditions who have activation of their sympathetic nervous system and catecholamines release- they develop TTS as a complication of their primary condition or its treatment. There are several hypotheses concerning the cause of the disease. They include a decrease in estrogen levels; microcirculation dysfunction; endothelial dysfunction and the hypothesis based on the importance of the brain-heart axis. More and more research concerns the importance of genetic factors in the development of the disease. To date; no effective treatment or prevention of recurrent TTS has been found. Only when the pathophysiology of the disease is fully known; then personalized treatment will be possible.

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