Document Detail


Adverse cardiac remodelling in spontaneously hypertensive rats: acceleration by high aerobic exercise intensity.
MedLine Citation:
PMID:  22930266     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In the present study it was hypothesized that voluntary aerobic exercise favours a pro-fibrotic phenotype and promotes adverse remodelling in hearts from spontaneously hypertensive rats (SHRs) in an angiotensin II-dependent manner. To test this, female SHRs at the age of 1 year were started to perform free running wheel exercise. Captopril was used to inhibit the renin-angiotensin system (RAS). Normotensive rats and SHRs kept in regular cages were used as sedentary controls. Training intensity, expressed as mean running velocity, was positively correlated with the left ventricular mRNA expression of TGF-β(1), collagen-III and biglycan but negatively correlated with the ratio of sarcoplasmic reticulum Ca(2+)-ATPase (SERCA)2a to Na(+)-Ca(2+) exchanger (NCX). A pro-fibrotic phenotype was verified by Picrosirius red staining. Sixty-seven per cent of SHRs performing free running wheel exercise died either spontaneously or had to be killed during a 6 month follow-up. In the presence of captopril, aerobic exercise did not show a similar positive correlation between training intensity and the expression of fibrotic markers. Moreover, in SHRs receiving captopril and performing free running wheel exercise, a training intensity-dependent reverse remodelling of the SERCA2a-to-NCX ratio was observed. None of these rats died spontaneously or had to be killed. In captopril-treated SHRs performing exercise, expression of mRNA for decorin, a natural inhibitor of TGF-β(1), was up-regulated. Despite these differences between SHR-training groups with and without captopril, positive training effects (lower resting heart rate and no progression of hypertension) were found in both groups. In conclusion, high aerobic exercise induces an angiotensin II-dependent adverse remodelling in chronic pressure overloaded hearts. However, high physical activity can potentially induce reverse remodelling in the presence of RAS inhibition.
Authors:
Rui Manuel da Costa Rebelo; Rolf Schreckenberg; Klaus-Dieter Schlüter
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-08-28
Journal Detail:
Title:  The Journal of physiology     Volume:  590     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2012 Nov 
Date Detail:
Created Date:  2012-11-02     Completed Date:  2013-03-25     Revised Date:  2013-11-05    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  5389-400     Citation Subset:  IM    
Affiliation:
Justus-Liebig Universität, Physiologisches Institut, Aulweg 129, 35392 Giessen, Germany. klaus-dieter.schlueter@physiologie.med.uni-giessen.de
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MeSH Terms
Descriptor/Qualifier:
Angiotensin II / physiology*
Angiotensin-Converting Enzyme Inhibitors / pharmacology
Animals
Antihypertensive Agents / pharmacology
Captopril / pharmacology
Female
Hypertension / physiopathology*
Physical Conditioning, Animal / physiology*
Rats
Rats, Inbred SHR
Rats, Wistar
Risk Factors
Ventricular Remodeling / physiology*
Chemical
Reg. No./Substance:
0/Angiotensin-Converting Enzyme Inhibitors; 0/Antihypertensive Agents; 11128-99-7/Angiotensin II; 62571-86-2/Captopril
Comments/Corrections
Comment In:
J Physiol. 2013 Apr 15;591(Pt 8):2025-6   [PMID:  23588501 ]
J Physiol. 2013 Apr 15;591(Pt 8):2225-6   [PMID:  23588504 ]
J Physiol. 2013 Apr 15;591(Pt 8):2227-8   [PMID:  23588505 ]

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