Document Detail

Regression of cardiac hypertrophy with drug treatment in spontaneously hypertensive rats.
MedLine Citation:
PMID:  6152298     Owner:  NLM     Status:  MEDLINE    
Left ventricular hypertrophy is an important complication of essential hypertension. Some antihypertensive drugs have been shown to allow regression of cardiac hypertrophy, both in spontaneously hypertensive rats and in hypertensive patients. Recent results show that the agents which interfere with the functions of the sympathetic nervous system, converting enzyme inhibitors and calcium antagonists are effective in reducing arterial blood pressure and regression of left ventricular hypertrophy. The use of vasodilators and diuretics may under certain circumstances, however, even exacerbate cardiac hypertrophy. Regression of left ventricular hypertrophy in hypertension does not appear to depend solely on reduction of arterial blood pressure. Other factors seem to modulate the myocardial response to antihypertensive treatment. Included among these mechanisms are neural, humoral, haemodynamic and biochemical factors. The available experimental data further suggest that some functional derangements and biochemical changes associated with hypertrophy may be reversed by antihypertensive treatment. There is, however, insufficient experience with human subjects to determine whether a reduction in left ventricular mass is associated with lower incidences of heart failure or mortality than may be achieved by adequate blood pressure control alone.
H Ruskoaho
Related Documents :
17210838 - Cardiac and systemic hemodynamic characteristics of hypertension and prehypertension in...
12016628 - Continuous ambulatory right heart pressure measurements with an implantable hemodynamic...
7010978 - Cardiovascular disturbances in chronic respiratory insufficiency.
12640508 - Mildly symptomatic chronic mitral regurgitation. analysis of left ventricular systolic ...
6639508 - Combined trabeculectomy and cataract extraction.
564028 - The effect of elevated outflow pressure on flow resistance and the transfer of tho, alb...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Medical biology     Volume:  62     ISSN:  0302-2137     ISO Abbreviation:  Med. Biol.     Publication Date:  1984  
Date Detail:
Created Date:  1985-04-29     Completed Date:  1985-04-29     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0417300     Medline TA:  Med Biol     Country:  FINLAND    
Other Details:
Languages:  eng     Pagination:  263-76     Citation Subset:  IM    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Adrenergic alpha-Antagonists / therapeutic use
Adrenergic beta-Antagonists / therapeutic use
Antihypertensive Agents / therapeutic use*
Blood Pressure / drug effects
Cardiomegaly / drug therapy*,  etiology,  physiopathology
Catecholamines / physiology
Collagen / analysis
Diuretics / therapeutic use
Heart / physiopathology
Hypertension / complications*,  physiopathology
Methyldopa / therapeutic use
Myocardium / analysis
Myosins / analysis
Ornithine Decarboxylase / metabolism
Polyamines / analysis
Rats, Inbred SHR
Vascular Resistance
Vasodilator Agents / therapeutic use
Reg. No./Substance:
0/Adrenergic alpha-Antagonists; 0/Adrenergic beta-Antagonists; 0/Antihypertensive Agents; 0/Catecholamines; 0/Diuretics; 0/Polyamines; 0/Vasodilator Agents; 555-30-6/Methyldopa; 9007-34-5/Collagen; EC; EC Decarboxylase

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

Previous Document:  Erythrocyte membrane ATPase activity of G6PD-deficient individuals and the effect of primaquine meta...
Next Document:  Erythema nodosum and Crohn's disease