Document Detail

Chronic all-trans retinoic acid treatment prevents medial thickening of intramyocardial and intrarenal arteries in spontaneously hypertensive rats.
MedLine Citation:
PMID:  12775563     Owner:  NLM     Status:  MEDLINE    
There are in vitro data linking all-trans retinoic acid (atRA) with inhibition of hypertrophy and hyperplasia in cardiomyocytes, vascular smooth muscle cells, and fibroblasts. In the present study, we tested the hypothesis that chronic treatment with atRA may blunt the process of myocardial remodeling in spontaneously hypertensive rats (SHR). Four-week-old male SHR were treated with atRA (5 or 10 given daily for 3 mo by gavage; age- and sex-matched Wistar-Kyoto rats (WKY) and placebo-treated SHR served as controls. At the end of the treatment period, cardiac geometry and function were assessed by Doppler echocardiography. Histological examination and RIA were performed to evaluate medial thickening of intramyocardial and renal arteries, perivascular and interstitial collagen content, and atrial natriuretic peptide (ANP) and IGF-I in the heart, respectively. The novel finding of the present study is that atRA prevented hypertrophy of intramyocardial and intrarenal arteries and ventricular fibrosis. However, atRA treatment did not lower blood pressure or left ventricular weight and left ventricular weight-to-body weight ratio in SHR. atRA did not change cardiac geometry and function as assessed by Doppler echocardiography. atRA showed no influence on either ANP or IGF-I levels. In conclusion, the present study suggests that chronic atRA treatment prevents medial thickening of intramyocardial and intrarenal arteries and ventricular fibrosis during the development of hypertension. Left ventricular hypertrophy and cardiac geometry and function are not changed by atRA treatment.
Lei Lü; Tai Yao; Yi-Zhun Zhu; Guo-Ying Huang; Yin-Xiang Cao; Yi-Chun Zhu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2003-05-29
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  285     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2003 Oct 
Date Detail:
Created Date:  2003-09-12     Completed Date:  2003-10-10     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1370-7     Citation Subset:  IM    
Department of Physiology and Pathophysiology, Key Laboratory of Molecular Medicine of the Ministry of Education, Fudan University Shanghai Medical College, 138 Yi Xue Yuan Rd., Shanghai 200032, People's Republic of China.
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MeSH Terms
Body Weight / drug effects
Coronary Vessels / drug effects*,  pathology
Drug Administration Schedule
Heart / drug effects
Heart Ventricles
Hemodynamics / drug effects
Hypertension / pathology,  physiopathology*
Myocardium / pathology
Organ Size / drug effects
Rats, Inbred SHR
Rats, Inbred WKY
Renal Artery / drug effects*,  pathology
Tretinoin / administration & dosage*
Tunica Media / drug effects*,  pathology
Reg. No./Substance:

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

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