Document Detail


The 'neuroadrenergic hypothesis' in hypertension: current evidence.
MedLine Citation:
PMID:  20008032     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Data collected in experimental animals and in humans support the hypothesis that sympathetic neural mechanisms are involved in the development and progression of hypertension. Direct approaches to assess human adrenergic cardiovascular drive have shown that sympathetic activation occurs in hypertensive patients, the magnitude of which is proportional to the degree of elevation of the blood pressure. Evidence has also been obtained that sympathetic activation participates in the development of hypertension-related target organ damage, such as left ventricular diastolic dysfunction, left ventricular hypertrophy and arterial remodelling and hypertrophy. Despite the large amount of information collected on the main features of the hypertension-related neurogenic abnormality, the causes of the sympathetic activation remain undefined, although alterations in the reflex modulation of adrenergic drive and/or participation of metabolic factors are likely candidates. This paper will provide background information on the behaviour of the sympathetic nervous system in experimental hypertension, followed by a review of the main features, mechanisms and effects of the sympathetic overdrive in human hypertension. Finally, the new frontiers of research in the area of therapeutic intervention aimed at reducing the adrenergic overdrive will be highlighted.
Authors:
Guido Grassi; Gino Seravalle; Fosca Quarti-Trevano
Publication Detail:
Type:  Journal Article; Review     Date:  2009-12-11
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:  -    
Medline Journal Info:
Nlm Unique ID:  9002940     Medline TA:  Exp Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  581-6     Citation Subset:  IM    
Affiliation:
Clinica Medica, Ospedale S. Gerardo dei Tintori, Via Pergolesi 33, 20052 Monza, Milan, Italy. guido.grassi@unimib.it
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Baroreflex / physiology
Disease Models, Animal
Humans
Hypertension / physiopathology*
Hypertrophy / physiopathology
Hypertrophy, Left Ventricular / physiopathology
Muscle, Smooth, Vascular / physiopathology
Norepinephrine / physiology
Sympathetic Nervous System / physiopathology*
Ventricular Dysfunction, Left / physiopathology
Chemical
Reg. No./Substance:
51-41-2/Norepinephrine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Enhanced Survival of Vascular Smooth Muscle Cells Accounts for Heightened Elastin Deposition in Arte...
Next Document:  Myricetin inhibits UVB-induced angiogenesis by regulating PI-3 kinase in vivo.