Document Detail


Therapeutic strategies for targeting excessive central sympathetic activation in human hypertension.
MedLine Citation:
PMID:  20304932     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The pathogenesis of hypertension and its mode of progression are complex, multifactoral and incompletely understood. However, there is accumulating evidence from humans and animal models of hypertension indicating that excessive central sympathetic nerve activity (SNA) plays a pathogenic role in triggering and sustaining the essential hypertensive state (the so-called 'neuroadrenergic hypothesis'). Importantly, augmented central sympathetic outflow has also been implicated in the initiation and progression of a plethora of pathophysiological processes independent of any increase in blood pressure, such as left ventricular hypertrophy and cardiac arrhythmias. Thus, the sympathetic nervous system constitutes an important putative drug target in hypertension. However, traditional pharmacological approaches for the management of essential hypertension appear ineffective in reducing central sympathetic outflow. Recently, several new and promising therapeutic strategies targeting neurogenic hypertension have been developed. The present report will provide a brief update of this topic with a particular emphasis on human studies examining the efficacy of novel pharmacological approaches (central sympatholytics and statins), lifestyle modification (aerobic exercise training, weight loss and stress reduction) and surgical intervention (renal denervation, chronic carotid baroreflex stimulation and deep brain stimulation) in reducing excessive central sympathetic activation in hypertension.
Authors:
James P Fisher; Paul J Fadel
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-03-19
Journal Detail:
Title:  Experimental physiology     Volume:  95     ISSN:  1469-445X     ISO Abbreviation:  Exp. Physiol.     Publication Date:  2010 May 
Date Detail:
Created Date:  2010-04-21     Completed Date:  2010-07-12     Revised Date:  2014-09-21    
Medline Journal Info:
Nlm Unique ID:  9002940     Medline TA:  Exp Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  572-80     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Antihypertensive Agents / therapeutic use
Baroreflex / physiology
Denervation
Electric Stimulation Therapy
Exercise
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use
Hypertension / drug therapy*,  physiopathology
Kidney / innervation
Nitric Oxide / physiology
Nitric Oxide Synthase / antagonists & inhibitors
Reactive Oxygen Species / antagonists & inhibitors
Stress, Psychological
Sympathetic Nervous System / drug effects,  physiopathology
Sympatholytics / therapeutic use
Weight Loss
Grant Support
ID/Acronym/Agency:
DK-076636/DK/NIDDK NIH HHS; R21 DK076636/DK/NIDDK NIH HHS; R21 DK076636-02/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Antihypertensive Agents; 0/Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0/Reactive Oxygen Species; 0/Sympatholytics; 31C4KY9ESH/Nitric Oxide; EC 1.14.13.39/Nitric Oxide Synthase
Comments/Corrections

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