Document Detail

Antihypertensive agents that limit ventricular hypertrophy inhibit cardiac expression of insulin-like growth factor-I.
MedLine Citation:
PMID:  9444886     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Left ventricular hypertrophy (LVH) is a generalized adaptation to altered myocardial load. Hypertension induces significant increases in ventricular IGF-I gene expression that occur coordinately with development of LVH. To test whether IGF-I promotes initiation of LVH, we examined ventricular IGF-I mRNA content in spontaneously hypertensive rats (SHRs) treated with antihypertensive drugs that limit or permit LVH. METHODS: Prehypertensive SHRs were left untreated or treated with enalapril, nifedipine, or hydralazine. Systolic blood pressure (SBP), hypertrophy index (ventricular weight/body weight), and ventricular IGF-I mRNA levels were examined 2, 4, and 6 weeks after beginning therapy in the experimental groups. RESULTS: Systolic blood pressure reached hypertensive levels after 2 weeks in untreated animals, and was controlled in the treated animals. The hypertrophy index in untreated animals was significantly elevated at 4 weeks. By 6 weeks, the hypertrophy indices of both the enalapril- and nifedipine-treated groups were significantly lower than that of the untreated group. In contrast, the hypertrophy index of the hydralazine-treated animals remained comparable to that of the untreated animals. By 4 weeks, IGF-I mRNA levels in the enalapril- and nifedipine-treated groups were significantly lower than those in the untreated and hydralazine-treated groups. CONCLUSIONS: We conclude that: (1) antihypertensive drugs that reduce LVH blunt ventricular IGF-I mRNA content; and (2) the hemodynamic effects of antihypertensives may be dissociated from their ability to promote or limit a hypertrophic response. The clear association of LVH with ventricular IGF-I mRNA content suggests that IGF-I is an important determinant of ventricular growth. Our data also suggest that angiotensin-converting enzyme inhibitors and calcium channel blockers may reduce LVH by inhibiting cardiac IGF-I gene expression.
T J Donohue; L D Dworkin; J Ma; M N Lango; V M Catanese
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of investigative medicine : the official publication of the American Federation for Clinical Research     Volume:  45     ISSN:  1081-5589     ISO Abbreviation:  J. Investig. Med.     Publication Date:  1997 Dec 
Date Detail:
Created Date:  1998-02-12     Completed Date:  1998-02-12     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  9501229     Medline TA:  J Investig Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  584-91     Citation Subset:  IM    
Division of Molecular Endocrinology, New York University School of Medicine, New York 10016, USA.
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MeSH Terms
Antihypertensive Agents / therapeutic use*
Blood Pressure / drug effects
Enalapril / therapeutic use
Heart / drug effects*
Hydralazine / therapeutic use
Hypertension / drug therapy*
Hypertrophy, Left Ventricular / metabolism,  prevention & control*
Insulin-Like Growth Factor I / metabolism*
Myocardium / metabolism*,  pathology
Nifedipine / therapeutic use
Organ Size / drug effects
RNA, Messenger / biosynthesis,  drug effects
Rats, Inbred SHR
Reg. No./Substance:
0/Antihypertensive Agents; 0/RNA, Messenger; 21829-25-4/Nifedipine; 67763-96-6/Insulin-Like Growth Factor I; 75847-73-3/Enalapril; 86-54-4/Hydralazine

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

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