alexa Adrenergic Nervous System and Hemostasis | OMICS International
ISSN: 2329-8790
Journal of Hematology & Thromboembolic Diseases
Make the best use of Scientific Research and information from our 700+ peer reviewed, Open Access Journals that operates with the help of 50,000+ Editorial Board Members and esteemed reviewers and 1000+ Scientific associations in Medical, Clinical, Pharmaceutical, Engineering, Technology and Management Fields.
Meet Inspiring Speakers and Experts at our 3000+ Global Conferenceseries Events with over 600+ Conferences, 1200+ Symposiums and 1200+ Workshops on
Medical, Pharma, Engineering, Science, Technology and Business

Adrenergic Nervous System and Hemostasis

Gennaro Pagano1*, Graziamaria Corbi2 and Nicola Ferrara1,3
1Division of Geriatrics, Department of Translational Medical Sciences, Federico II University of Naples, Italy
2Department of Medicine and Health Sciences, University of Molise, Italy
3Division of Cardiology, Salvatore Maugeri Foundation, IRCCS, Scientific Institute of Telese Terme (BN), Italy
Corresponding Author : Pagano Gennaro
Division of Geriatrics
Department of Translational Medical Sciences Federico II University
Via Pansini 5, 80131 Naples, Italy
Tel: +39-081-7462277
E-mail: [email protected]
Received February 05, 2014; Accepted February 07, 2014; Published February 12, 2014
Citation: Pagano G, Corbi G, Ferrara N (2014) Adrenergic Nervous System and Hemostasis. J Hematol Thrombo Dis 2:e108. doi: 10.4172/2329-8790.1000e108
Copyright: © 2014 Pagano Gennaro et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Related article at
DownloadPubmed DownloadScholar Google

Visit for more related articles at Journal of Hematology & Thromboembolic Diseases

Abstract

Hemostatic processes contribute to gradual fibrin deposition within atherosclerotic plaques and overt thrombus formation subsequent to plaque disruption. Activation of sympathetic nervous system (SNS) affects blood coagulation, fibrinolysis and platelet activation by several mechanisms.

Given the significance of increased hemostatic activity in atherosclerosis and thrombosis and the important role of the SNS in cardiovascular disease, sympathetic activation and catecholamine effects might contribute to arterial thrombus formation.

In particular, chronic stimulation of the SNS and concomitant hypercoagulable changes could contribute to gradual fibrin deposition at sites of atherosclerotic lesions and, in patients with endothelial dysfunction, acute stress response could trigger rupture of an atherosclerotic plaque.

Further studies are needed to better understanding the regulation of the SNS-hemostasis axis.

Abstract
Hemostatic processes contribute to gradual fibrin deposition within atherosclerotic plaques and overt thrombus formation subsequent to plaque disruption. Activation of sympathetic nervous system (SNS) affects blood coagulation, fibrinolysis and platelet activation by several mechanisms.
Given the significance of increased hemostatic activity in atherosclerosis and thrombosis and the important role of the SNS in cardiovascular disease, sympathetic activation and catecholamine effects might contribute to arterial thrombus formation.
In particular, chronic stimulation of the SNS and concomitant hypercoagulable changes could contribute to gradual fibrin deposition at sites of atherosclerotic lesions and, in patients with endothelial dysfunction, acute stress response could trigger rupture of an atherosclerotic plaque.
Further studies are needed to better understanding the regulation of the SNS-hemostasis axis.
Keywords
Sympathetic nervous system; Hemostasis; Blood coagulation; Fibrinolysis; Platelet activation; Fight-or-flight response
Introduction
Hemostatic processes contribute to gradual fibrin deposition within atherosclerotic plaques and overt thrombus formation subsequent to plaque disruption [1]. It is still debated whether hypercoagulability indicates an underlying atherosclerotic process or is cause of atherosclerosis and thrombosis [2]. Stimulation of sympathetic nervous system (SNS) increases blood clotting (by V, VIII, and Von Willebrand factors) and platelet activation with raised risk for atherothrombotic events [3-12]. The SNS regulates several homeostatic functions (e.g. cardiac, respiratory, digestion, urination, and sexual arousal) and induces physiological changes during the “fight-or-flight response”(also called the acute stress response), that is a physiological reaction occurring in response to a perceived harmful event, attack, or threat to survival [13].
During acute stress response, catecholamines (adrenaline and noradrenaline) facilitate immediate physical reactions associated with a preparation for violent muscular action and increased strength and speed in anticipation of fighting or running. These physiological changes include: increased blood flow to the muscles, raised blood pressure, heart rate, blood sugars, and fats, increased muscle tension, dilation of pupil, enhanced perspiration and increase the blood clotting function of the body speeds up [14-16] (Figure 1).
Although hastened blood coagulation the impact of SNS activation on hemostasis is not still clearly understood.
Adrenergic nervous system and hemostasis
Given the significance of increased hemostatic activity in atherosclerosis and the important role of the SNS in cardiovascular disease [17], SNS activation might contribute to arterial thrombus formation. Several studies have demonstrated that SNS activation induced procoagulant responses in patients with atherosclerotic plaques and endothelial dysfunction [18-24]. Adrenaline infusion induces platelet activity and it is higher in hypertensive individuals than in normotensive controls [25-27]. Moreover behavioral stressors, such as mental arithmetic an cold test, led to increase in fibrinogen [28] and platelet activity [29] as well as to impaired fibrinolysis [28,30] in hypertensive individuals compared with normotensive controls. In patients with heart failure, there is an higher platelet activity with acute mental stress than normal controls [31].
Chronic stimulation of the SNS and concomitant hypercoagulable changes could contribute to gradual fibrin deposition at sites of atherosclerotic lesions. Once hemodynamic stress with for instance emotional arousal has triggered rupture of an atherosclerotic plaque [32,33], hypercoagulability due to catecholamine spillover with both activation of the hypothalamic-pituitary-adrenal axis [34] and myocardial ischemia [35-36] may promote coronary thrombus growth. Also, hypercoagulable changes with morning surge in catecholamine levels due to both circadian variation in catecholamine activity and postural change may be related to increased morning frequencies of thrombotic vascular events [37-39].
Conclusion
Future studies on the effects of SNS function on hemostasis mechanisms may further help integrating arduously achieved biochemical and biological knowledge to a better understanding of the regulation of the SNS-hemostasis axis [40].
References








































Figures at a glance

image
Figure 1
Select your language of interest to view the total content in your interested language
Post your comment

Share This Article

Relevant Topics

Recommended Conferences

  • International Conference on Medical and Health Science
    August 24-25, 2018 Tokyo, Japan
  • 9th International Conference on Clinical & Medical Case Reports
    September 17-18, 2018 Amsterdam, Netherlands
  • 8th International Congress on Health and Medicine
    October 08-09, 2018 Osaka, Japan
  • 3rd International Conference on Integrative Medicine and Alternative treatments
    October 22-23, 2018 Boston, USA

Article Usage

  • Total views: 12051
  • [From(publication date):
    March-2014 - Jul 20, 2018]
  • Breakdown by view type
  • HTML page views : 8228
  • PDF downloads : 3823
 

Post your comment

captcha   Reload  Can't read the image? click here to refresh

Peer Reviewed Journals
 
Make the best use of Scientific Research and information from our 700 + peer reviewed, Open Access Journals
International Conferences 2018-19
 
Meet Inspiring Speakers and Experts at our 3000+ Global Annual Meetings

Contact Us

Agri & Aquaculture Journals

Dr. Krish

[email protected]

+1-702-714-7001Extn: 9040

Biochemistry Journals

Datta A

[email protected]

1-702-714-7001Extn: 9037

Business & Management Journals

Ronald

[email protected]

1-702-714-7001Extn: 9042

Chemistry Journals

Gabriel Shaw

[email protected]

1-702-714-7001Extn: 9040

Clinical Journals

Datta A

[email protected]

1-702-714-7001Extn: 9037

Engineering Journals

James Franklin

[email protected]

1-702-714-7001Extn: 9042

Food & Nutrition Journals

Katie Wilson

[email protected]

1-702-714-7001Extn: 9042

General Science

Andrea Jason

[email protected]

1-702-714-7001Extn: 9043

Genetics & Molecular Biology Journals

Anna Melissa

[email protected]

1-702-714-7001Extn: 9006

Immunology & Microbiology Journals

David Gorantl

[email protected]

1-702-714-7001Extn: 9014

Materials Science Journals

Rachle Green

[email protected]

1-702-714-7001Extn: 9039

Nursing & Health Care Journals

Stephanie Skinner

[email protected]

1-702-714-7001Extn: 9039

Medical Journals

Nimmi Anna

[email protected]

1-702-714-7001Extn: 9038

Neuroscience & Psychology Journals

Nathan T

[email protected]

1-702-714-7001Extn: 9041

Pharmaceutical Sciences Journals

Ann Jose

[email protected]

1-702-714-7001Extn: 9007

Social & Political Science Journals

Steve Harry

[email protected]

1-702-714-7001Extn: 9042

 
© 2008- 2018 OMICS International - Open Access Publisher. Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version