Document Detail


Abnormal baroreflex function is dissociated from central angiotensin II receptor expression in chronic heart failure.
MedLine Citation:
PMID:  22258229     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Neurohumoral disturbances characterize chronic heart failure (CHF) and are reflected, in part, as impairment of baroreflex sensitivity (BRS) and sympathetic function. However, the mechanisms that trigger these neurohumoral abnormalities in CHF are not clear. We hypothesized that the BRS is blunted early in CHF and that the humoral effects occur later and contribute to progressive loss of cardiovascular control in CHF. We assessed the BRS (beats/min per mmHg) and recorded renal sympathetic nerve activity (RSNA) in four groups of conscious rabbits at varying time intervals: control, 1-week CHF, 2-week CHF, and 3-week CHF. Chronic heart failure was induced by ventricular pacing at 360 beats/min and was assessed by echocardiography. Arterial blood pressure and heart rate were recorded by an implanted telemetric device and RSNA through an implanted electrode. A significant fall in the ejection fraction, fractional shortening, and an increase in left ventricular end-systolic diameter and left ventricular end-diastolic diameter were observed in all CHF groups. The BRS was significantly reduced in all the CHF groups with no significant change in the basal RSNA (% of maximum) after 1 week of pacing; a small but insignificant rise in RSNA was seen at 2 weeks, and a significant rise in RSNA was observed at 3 weeks. Angiotensin II type 1 (AT-1) receptor protein (Western Blot) and mRNA (reverse transcriptase-polymerase chain reaction) expression in the rostral ventrolateral medulla exhibited a progressive increase with the duration of CHF, reaching significance after 3 weeks, the same time point in which RSNA was significantly elevated. These data are the first to examine early changes in central AT-1 receptors in CHF and suggest that the fall in BRS and hemodynamic changes occur early in the development of CHF followed by sympathoexcitation and overexpression of AT-1 receptors with the progression of CHF, causing further impairment of cardiovascular control.
Authors:
Mohammad Fahim; Lie Gao; Tarek M Mousa; Dongmei Liu; Kurtis G Cornish; Irving H Zucker
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Shock (Augusta, Ga.)     Volume:  37     ISSN:  1540-0514     ISO Abbreviation:  Shock     Publication Date:  2012 Mar 
Date Detail:
Created Date:  2012-02-16     Completed Date:  2012-06-19     Revised Date:  2014-09-08    
Medline Journal Info:
Nlm Unique ID:  9421564     Medline TA:  Shock     Country:  United States    
Other Details:
Languages:  eng     Pagination:  319-24     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Angiotensin II / blood
Animals
Baroreflex / physiology*
Heart Failure / etiology,  physiopathology*
Hemodynamics / physiology
Kidney / innervation
Male
Membrane Glycoproteins / biosynthesis
NADPH Oxidase / biosynthesis
Rabbits
Receptor, Angiotensin, Type 1 / biosynthesis*,  physiology
Sympathetic Nervous System / physiology
Grant Support
ID/Acronym/Agency:
P0-1HL-62222/HL/NHLBI NIH HHS; P01 HL062222/HL/NHLBI NIH HHS; P01 HL062222-13/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Membrane Glycoproteins; 0/Receptor, Angiotensin, Type 1; 11128-99-7/Angiotensin II; EC 1.6.3.1/NADPH Oxidase
Comments/Corrections

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


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