Enhanced cardiac angiotensinogen gene expression and angiotensin converting enzyme activity in tachypacing-induced heart failure in rats

The aim of the study was to analyze changes in myocardial angiotensinogen gene expression and myocardial angiotensin converting enzyme activity in slowly progressing low-output failure. In adult, male Wistar rats, acute ventricular tachypacing by 610 to 620 impulses per minute lowered end-diastolic...

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Bibliographic Details
Published in:Basic research in cardiology 1991-07, Vol.86 (4), p.303-316
Main Authors: FINCKH, M, HELLMANN, W, GANTEN, D, FURTWANGLER, A, ALLGEIER, J, BOLTZ, M, HOLTZ, J
Format: Article
Language:English
Subjects:
Angiotensinogen - biosynthesis
Angiotensinogen - genetics
Animals
Biological and medical sciences
Cardiac Output, Low - metabolism
Cardiac Pacing, Artificial
Cardiology. Vascular system
Gene Expression Regulation
Heart
Heart failure, cardiogenic pulmonary edema, cardiac enlargement
Hemodynamics
Male
Medical sciences
Peptidyl-Dipeptidase A - metabolism
Rats
Rats, Inbred Strains
RNA, Messenger - analysis
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Summary:The aim of the study was to analyze changes in myocardial angiotensinogen gene expression and myocardial angiotensin converting enzyme activity in slowly progressing low-output failure. In adult, male Wistar rats, acute ventricular tachypacing by 610 to 620 impulses per minute lowered end-diastolic external diameter of the left ventricle by 2.6% (p less than 0.01), but did not lower cardiac output or abolish coronary reserve, since left-ventricular subendocardial blood flow of paced rats increased under dipyridamole (2 mg/kg i.v.) by 56% (p less than 0.01). Systemic neuroendocrine activation and ventricular dilation without enlargement of ventricular mass developed subsequent to chronic tachypacing, but left-ventricular diameter during pacing never exceeded the value of sham rats on sinus rhythm. After 2 weeks, cardiac output was lowered by 14% (p less than 0.001), cardiopulmonary blood volume was elevated by 30% (p less than 0.001), and angiotensinogen mRNA and angiotensin converting enzyme activity in ventricular myocardium were doubled. We conclude that conditions for an enhanced intracardiac angiotensin II-formation developed in tachypacing-induced heart failure, but that enhanced systolic wall stress or myocardial ischemia are not required for this activation of the local cardiac renin-angiotensin system.
ISSN:0300-8428
1435-1803
DOI:10.1007/bf02191528