Document Detail


Mechanisms of abnormal renal sodium handling in obesity hypertension.
MedLine Citation:
PMID:  9160781     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Obesity-induced hypertension, like all forms of experimental and human hypertension studied thus far, is associated with renal dysfunction characterized by the resetting of pressure natriuresis. In obese subjects, this resetting is primarily a result of increased renal tubular reabsorption as glomerular filtration rate and renal blood flow are markedly elevated. Obesity activates the sympathetic nervous and renin-angiotensin systems, and causes insulin resistance and hyperinsulinemia, all of which have been postulated to increase tubular reabsorption and raise blood pressure. In humans and dogs, chronic hyperinsulinemia, comparable to that found in obesity, does not cause hypertension even in the presence of insulin resistance. Activation of the sympathetic nervous system appears to be important in obesity, as chronic adrenergic blockade or renal denervation greatly ameliorates the hypertension associated with weight gain. Resetting of pressure natriuresis in obesity may also be attributable to altered intrarenal forces caused by histologic changes in the renal medulla that may compress the loops of Henle and vasa recta, increase tubular sodium reabsorption, and activate the renin-angiotensin system. The quantitative importance of these intrarenal changes and their interrelationship with neurohumoral activation in obesity is an important area for further investigation.
Authors:
J E Hall
Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  American journal of hypertension     Volume:  10     ISSN:  0895-7061     ISO Abbreviation:  Am. J. Hypertens.     Publication Date:  1997 May 
Date Detail:
Created Date:  1997-07-17     Completed Date:  1997-07-17     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:  49S-55S     Citation Subset:  IM    
Affiliation:
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Humans
Hyperinsulinism / etiology
Hypertension / etiology*,  physiopathology*
Insulin Resistance
Kidney / metabolism*
Natriuresis
Obesity / complications*,  physiopathology
Sodium / metabolism*
Sympathetic Nervous System / physiopathology
Grant Support
ID/Acronym/Agency:
HL 39399/HL/NHLBI NIH HHS; HL23502/HL/NHLBI NIH HHS; HL57971/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
7440-23-5/Sodium

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


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