Document Detail


The sympathetic system and hypertension.
MedLine Citation:
PMID:  10921528     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Measurement of regional sympathetic activity in lean essential hypertension patients using electrophysiologic (sympathetic nerve recording) and neurochemical (measurement of norepinephrine spillover) techniques demonstrates activation of sympathetic outflow to the heart, kidneys, and skeletal muscle vasculature in younger (< 45 years) patients. The increase in sympathetic activity is a mechanism for both initiating and sustaining the blood pressure elevation. Sympathetic nervous activation also confers specific cardiovascular risk. Stimulation of the sympathetic nerves to the heart promotes the development of left ventricular hypertrophy and contributes to the genesis of ventricular arrhythmias and sudden death. Sympathetically mediated vasoconstriction in skeletal muscle vascular beds reduces the uptake of glucose by muscle, and is thus a basis for insulin resistance and consequent hyperinsulinemia. Understanding the neural pathophysiology of obesity-related hypertension has been more difficult. In normotensive obesity, renal sympathetic tone is doubled, but cardiac norepinephrine spillover (a measure of sympathetic activity in the heart) is only 50% of normal. In obesity-related hypertension, there is a comparable elevation of renal norepinephrine spillover, but without suppression of cardiac sympathetics, as here cardiac norepinephrine spillover is more than double that of normotensive obese and 25% higher than in healthy volunteers. Increased renal sympathetic activity in obesity may be a necessary cause for the development of hypertension (predisposing to hypertension development), but apparently is not a sufficient cause. The discriminating feature of the obese who develop hypertension is the absence of the presumably adaptive suppression of cardiac sympathetic outflow seen in the normotensive obese. The sympathetic nervous system has moved towards center stage in cardiovascular medicine. The importance of sympathetic activation in heart failure progression and mortality and in the generation of ventricular arrhythmias is now well established. In essential hypertension also, although the mechanism differs somewhat between the lean and obese, the sympathetic nervous system is a key factor in the genesis of the disorder, and additionally promotes the development of complications. Through their central inhibition of sympathetic nervous activity, I1 agents such as rilmenidine powerfully reduce sympathetic nervous activity in essential hypertension patients, lowering blood pressure, and carrying the potential for specific cardiovascular protection.
Authors:
M Esler
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  American journal of hypertension     Volume:  13     ISSN:  0895-7061     ISO Abbreviation:  Am. J. Hypertens.     Publication Date:  2000 Jun 
Date Detail:
Created Date:  2000-11-06     Completed Date:  2000-11-15     Revised Date:  2009-02-24    
Medline Journal Info:
Nlm Unique ID:  8803676     Medline TA:  Am J Hypertens     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  99S-105S     Citation Subset:  IM    
Affiliation:
Baker Medical Research Institute, Prahran, Melbourne, Australia. esler@baker.edu.au
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MeSH Terms
Descriptor/Qualifier:
Antihypertensive Agents / therapeutic use
Blood Pressure
Humans
Hypertension / drug therapy,  physiopathology*
Norepinephrine / metabolism
Oxazoles / therapeutic use
Sympathetic Nervous System / drug effects,  physiopathology*
Chemical
Reg. No./Substance:
0/Antihypertensive Agents; 0/Oxazoles; 51-41-2/Norepinephrine; 54187-04-1/rilmenidine

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


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