Document Detail

Mechanical unloading versus neurohumoral stimulation on myocardial structure and endocrine function In vivo.
MedLine Citation:
PMID:  10899099     Owner:  NLM     Status:  MEDLINE    
BACKGROUND-Mechanical load and humoral stimuli such as endothelin (ET) and angiotensin II (Ang II) are potent modulators of cardiac structure and endocrine function, specifically gene expression and production and release of atrial natriuretic peptide (ANP). We define the contribution of mechanical load compared with neurohumoral stimulation in vivo with specific focus on myocardial and circulating ANP during chronic myocardial unloading produced by thoracic inferior vena caval constriction (TIVCC). METHODS AND RESULTS-TIVCC was produced by banding the IVC for 10 days in 7 dogs, whereas in the 6 control dogs, the band was not constricted. TIVCC was characterized by a decrease in cardiac output, right atrial pressure, and left ventricular (LV) end-diastolic diameter and marked activation of ET and Ang II in plasma and atrial and ventricular myocardium. Despite neurohumoral stimulation, LV mass index and myocyte diameters in unloaded hearts decreased, reflecting myocyte atrophy. The total number of myocytes in the LV remained unchanged. Atrial stores of ANP increased, but plasma ANP did not change, in association with a trend toward ANP gene expression to decrease in unloaded hearts. CONCLUSIONS-Chronic mechanical unloading of the heart results in myocardial atrophy and lack of activation of ANP synthesis despite marked neurohumoral stimulation by the growth promoters ET and Ang II.
O Lisy; M M Redfield; S Jovanovic; M Jougasaki; A Jovanovic; H Leskinen; A Terzic; J C Burnett
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Circulation     Volume:  102     ISSN:  1524-4539     ISO Abbreviation:  Circulation     Publication Date:  2000 Jul 
Date Detail:
Created Date:  2000-08-03     Completed Date:  2000-08-03     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  338-43     Citation Subset:  AIM; IM; S    
Division of Cardiovascular Diseases, Departments of Internal Medicine and Physiology, Mayo Clinic and Foundation, Rochester, MN, USA.
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MeSH Terms
Angiotensin II / pharmacology*
Atrial Natriuretic Factor / metabolism
Constriction, Pathologic
Endocrine Glands / physiology*
Endothelins / pharmacology*
Myocardium / metabolism,  pathology*
Neurotransmitter Agents / metabolism*
Stress, Mechanical
Vena Cava, Inferior
Grant Support
Reg. No./Substance:
0/Endothelins; 0/Neurotransmitter Agents; 11128-99-7/Angiotensin II; 85637-73-6/Atrial Natriuretic Factor

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