Insulin and the Regulation of the Cardiovascular System: Role of the l-arginine Nitric Oxide Pathway and the Sympathetic Nervous System

1995 ◽  
pp. 108-128 ◽  
Author(s):  
U. Scherrer
Keyword(s):  
Nitric Oxide ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Cardiovascular System ◽  
Sympathetic Nervous ◽  
Nitric Oxide Pathway

scholarly journals Role of leptin in energy expenditure: the hypothalamic perspective

2017 ◽  
Vol 312 (6) ◽  
pp. R938-R947 ◽  
Author(s):  
R. Pandit ◽  
S. Beerens ◽  
R. A. H. Adan
Keyword(s):  
Nervous System ◽  
Energy Expenditure ◽  
Sympathetic Nervous System ◽  
Cardiovascular System ◽  
Ventromedial Hypothalamus ◽  
Leptin Signaling ◽  
Hypothalamic Nuclei ◽  
Brown Adipose ◽  
Sympathetic Nervous

The adipocyte-derived hormone leptin is a peripheral signal that informs the brain about the metabolic status of an organism. Although traditionally viewed as an appetite-suppressing hormone, studies in the past decade have highlighted the role of leptin in energy expenditure. Leptin has been shown to increase energy expenditure in particular through its effects on the cardiovascular system and brown adipose tissue (BAT) thermogenesis via the hypothalamus. The current review summarizes the role of leptin signaling in various hypothalamic nuclei and its effects on the sympathetic nervous system to influence blood pressure, heart rate, and BAT thermogenesis. Specifically, the role of leptin signaling on three different hypothalamic nuclei, the dorsomedial hypothalamus, the ventromedial hypothalamus, and the arcuate nucleus, is reviewed. It is known that all of these brain regions influence the sympathetic nervous system activity and thereby regulate BAT thermogenesis and the cardiovascular system. Thus the current work focuses on how leptin signaling in specific neuronal populations within these hypothalamic nuclei influences certain aspects of energy expenditure.

Cardiac autonomic function in acutely nitric oxide deficient hypertensive rats: role of the sympathetic nervous system and oxidative stress

2011 ◽  
Vol 89 (12) ◽  
pp. 865-874 ◽  
Author(s):  
Meenakshi Chaswal ◽  
Shobha Das ◽  
Jagdish Prasad ◽  
Anju Katyal ◽  
Mohammad Fahim
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
High Frequency ◽  
Spectral Power ◽  
Pressor Response ◽  
Sympathetic Nervous ◽  
And Oxidative Stress

We evaluated the role of the sympathetic nervous system and oxidative stress in hemodynamic and autonomic control after acute inhibition of the synthesis of nitric oxide, using intravenous (i.v.) injection of 30 mg·kg–1 NG-nitro-l-arginine methyl ester (L-NAME) in adult Wistar rats. Baroreflex sensitivity (BRS) and heart rate variability (HRV) were measured as indices of cardiac autonomic control, before and after L-NAME treatment in rats with intact autonomic innervation, and in rats with chemical sympathectomy by 6-hydroxydopamine. Serum malondialdehyde (MDA) was measured as a marker of oxidative stress. In control rats, L-NAME treatment resulted in a significant rise in blood pressure, augmentation of BRS, and enhanced serum MDA. HRV showed an attenuation of total spectral power and high frequency spectral power, along with a rise of the low to high frequency ratio (LF:HF). Administration of L-NAME produced a pressor response even in sympathectomised rats, but augmented BRS was not observed, and the high frequency spectral power showed an increase, in addition to a significant decline of LF:HF and serum MDA. We therefore conclude that even though pressor response was unaffected, reversal of cardiac autonomic responses and decline in oxidative stress following sympathectomy in L-NAME-treated rats reflects a significant role for sympathetic innervation in acute L-NAME-induced hypertension.

scholarly journals The role of the vegetative part of sympathetic nervous system in development of cardiovascular complications in patients with arterial hypertension: pharmacological aspects

2014 ◽  
Vol 11 (3) ◽  
pp. 88-94
Author(s):  
S R Gilyarevsky
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Arterial Hypertension ◽  
Cardiovascular System ◽  
Antihypertensive Agents ◽  
Cardiovascular Complications ◽  
Autonomic Regulation ◽  
Sympathetic Nervous ◽  
The Impact

Recently, we have determined new interest in studying the role of sympathetic part of autonomic division of nervous system (SANS) in the pathogenesis of arterial hypertension (AH), as well as in studying the role of agents, suppressing the activity of SANS, using for AH treatment, including the usage of antihypertensive agents and non-pharmacological methods. This article discusses the changes of autonomic regulation of the cardiovascular system in patients with AH. The role of these changes in the development of the functional and structured changes of the heart and systemic vessels can be observing during long-standing AH and will lead to the development of adverse clinical outcomes. We have been showing received data, associated with the impact of non-medicated and pharmacological approaches to the autonomic regulation of the cardiovascular system.

Thyroid hormone-catecholamine interrelationships during exposure to cold

1981 ◽  
Vol 97 (1) ◽  
pp. 91-97 ◽  
Author(s):  
H. Storm ◽  
C. van Hardeveld ◽  
A. A. H. Kassenaar
Keyword(s):  
Nervous System ◽  
Plasma Concentration ◽  
Thyroid Hormone ◽  
Sympathetic Nervous System ◽  
Plasma Levels ◽  
Surgical Procedure ◽  
Exposure To Cold ◽  
Basal Plasma ◽  
Sympathetic Nervous

Abstract. Basal plasma levels for adrenalin (A), noradrenalin (NA), l-triiodothyronine (T3), and l-thyroxine (T4) were determined in rats with a chronically inserted catheter. The experiments described in this report were started 3 days after the surgical procedure when T3 and T4 levels had returned to normal. Basal levels for the catecholamines were reached already 4 h after the operation. The T3/T4 ratio in plasma was significantly increased after 3, 7, and 14 days in rats kept at 4°C and the same holds for the iodide in the 24-h urine after 7 and 14 days at 4°C. The venous NA plasma concentration was increased 6- to 12-fold during the same period of exposure to cold, whereas the A concentration remained at the basal level. During infusion of NA at 23°C the T3/T4 ratio in plasma was significantly increased after 7 days compared to pair-fed controls, and the same holds for the iodide excretion in the 24-h urine. This paper presents further evidence for a role of the sympathetic nervous system on T4 metabolism in rats at resting conditions.

Neurovascular Role of Sympathetic Nervous System and Beta-Adrenoceptor Polymorphisms in Obesity and Hypertension

2008 ◽  
Vol 4 (2) ◽  
pp. 121-130 ◽  
Author(s):  
Kazuko Masuo ◽  
Gavin Lambert ◽  
Hiromi Rakugi ◽  
Toshio Ogihara ◽  
Murray Esler
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Beta Adrenoceptor ◽  
Sympathetic Nervous

scholarly journals Pathophysiology of Resistant Hypertension: The Role of Sympathetic Nervous System

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Costas Tsioufis ◽  
Athanasios Kordalis ◽  
Dimitris Flessas ◽  
Ioannis Anastasopoulos ◽  
Dimitris Tsiachris ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Resistant Hypertension ◽  
Antihypertensive Treatment ◽  
Treatment Options ◽  
Treatment Resistance ◽  
Obstructive Sleep ◽  
Cardiovascular Morbidity And Mortality ◽  
Sympathetic Nervous

Resistant hypertension (RH) is a powerful risk factor for cardiovascular morbidity and mortality. Among the characteristics of patients with RH, obesity, obstructive sleep apnea, and aldosterone excess are covering a great area of the mosaic of RH phenotype. Increased sympathetic nervous system (SNS) activity is present in all these underlying conditions, supporting its crucial role in the pathophysiology of antihypertensive treatment resistance. Current clinical and experimental knowledge points towards an impact of several factors on SNS activation, namely, insulin resistance, adipokines, endothelial dysfunction, cyclic intermittent hypoxaemia, aldosterone effects on central nervous system, chemoreceptors, and baroreceptors dysregulation. The further investigation and understanding of the mechanisms leading to SNS activation could reveal novel therapeutic targets and expand our treatment options in the challenging management of RH.

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