The sympathetic nervous system (SNS) plays a key role in both cardiovascular and metabolic
regulation hence disturbances in SNS regulation are likely to impact on both cardiovascular
and metabolic health. With excess adiposity, in particular when visceral fat accumulation
is present, sympathetic activation commonly occurs. The cause and extent of sympathetic
activation in obesity may be attributed to factors such as the release of adipokines
from the adipose tissue, the existence of sleep apnoea, components of the metabolic
syndrome, distribution and type of fat and underlying stress. Sympathetic activation
may lead or further aggravate the elevation of blood pressure and end organ damage
including vascular, cardiac and renal impairment. Weight loss achieved by either lifestyle
changes including diet and exercise programs or bariatric surgery considerably decrease
sympathetic tone, improve the cardiovascular and metabolic profile of obese subjects
and decrease their cardiovascular risk. Whether some of the beneficial effects are
due to an inhibitory effect on sympathetic nervous activity is not known. Given the
lack of success in sustaining long term weight loss after diet or exercise the development
of interventions and strategies that optimise weight loss but also limit obesity related
cardio-metabolic disease development and progression is vital. Pharmacological and
device based approaches to directly or indirectly target the activation of the SNS
may offer some benefit in reducing the cardio-metabolic consequences of obesity.
To read this article in full you will need to make a payment
Purchase one-time access:
Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online accessOne-time access price info
- For academic or personal research use, select 'Academic and Personal'
- For corporate R&D use, select 'Corporate R&D Professionals'
Subscribe:
Subscribe to Autonomic Neuroscience: Basic and ClinicalAlready a print subscriber? Claim online access
Already an online subscriber? Sign in
Register: Create an account
Institutional Access: Sign in to ScienceDirect
Article info
Identification
Copyright
© 2015 Published by Elsevier Inc.