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Impaired relaxation of the hypertrophied myocardium is potentiated by angiotensin II.
Neyses, Ludwig; Vetter, H.
1989In Journal of Hypertension. Supplement), 7 (6), p. 104-5
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Keywords :
Angiotensin II/pharmacology; Animals; Cardiomegaly/physiopathology; Cells, Cultured/drug effects; Myocardial Contraction/drug effects; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Stimulation, Chemical
Abstract :
[en] Relaxation delay is an important feature of hypertensive heart disease which impairs diastolic coronary flow and ventricular filling and therefore contributes to heart failure. We investigated the hypothesis that impaired relaxation is a property of the myocardium, rather than the consequence of ischaemia or interstitial fibrosis. A new videomicroscope system was used to define the contraction-relaxation cycle of isolated cardiac myocytes from spontaneously hypertensive rats (SHR) and normotensive control (Wistar-Kyoto, WKY) rats. The SHR cells showed a marked relaxation delay. Angiotensin II (Ang II) increased the contraction maximum by about 35% in WKY rats and induced a relaxation delay. In SHR Ang II greatly potentiated this relaxation delay. Our results demonstrate that impairment of relaxation is a property of the single cardiomyocyte. Angiotensin II induces a relaxation delay that is independent of blood pressure. The combination of hypertrophy and high levels of Ang II potentiates relaxation impairment and may therefore contribute to hypertensive left ventricular failure.
Disciplines :
Cardiovascular & respiratory systems
Author, co-author :
Neyses, Ludwig ;  University of Luxembourg > Research Office
Vetter, H.
External co-authors :
yes
Language :
English
Title :
Impaired relaxation of the hypertrophied myocardium is potentiated by angiotensin II.
Publication date :
1989
Journal title :
Journal of Hypertension. Supplement)
ISSN :
0952-1178
Publisher :
Lippincott Williams & Wilkins, United States
Volume :
7
Issue :
6
Pages :
S104-5
Peer reviewed :
Peer Reviewed verified by ORBi
Available on ORBilu :
since 01 June 2016

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