| Therapeutic strategies for targeting excessive central sympathetic activation in human hypertension. | |
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MedLine Citation:
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PMID: 20304932 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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James P Fisher; Paul J Fadel |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2010-03-19 |
Journal Detail:
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Title: Experimental physiology Volume: 95 ISSN: 1469-445X ISO Abbreviation: Exp. Physiol. Publication Date: 2010 May |
Date Detail:
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Created Date: 2010-04-21 Completed Date: 2010-07-12 Revised Date: 2013-05-29 |
Medline Journal Info:
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Nlm Unique ID: 9002940 Medline TA: Exp Physiol Country: England |
Other Details:
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Languages: eng Pagination: 572-80 Citation Subset: IM |
Affiliation:
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School of Sport and Exercise Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK. j.p.fisher@bham.ac.uk |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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DK-076636/DK/NIDDK NIH HHS; R21 DK076636-02/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antihypertensive Agents; 0/Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0/Reactive Oxygen Species; 0/Sympatholytics; 10102-43-9/Nitric Oxide; EC 1.14.13.39/Nitric Oxide Synthase |
| Comments/Corrections | |
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