Increased cardiac angiotensin II levels induce right and left ventricular hypertrophy in normotensive mice.
Details
Serval ID
serval:BIB_4FE360B42251
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Increased cardiac angiotensin II levels induce right and left ventricular hypertrophy in normotensive mice.
Journal
Hypertension
ISSN
0194-911X
Publication state
Published
Issued date
2000
Peer-reviewed
Oui
Volume
35
Number
4
Pages
985-91
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't - Publication Status: ppublish
Abstract
Angiotensin II is a potent arterial vasoconstrictor and induces hypertension. Angiotensin II also exerts a trophic effect on cardiomyocytes in vitro. The goals of the present study were to document an in vivo increase in cardiac angiotensins in the absence of elevated plasma levels or hypertension and to investigate prevention or regression of ventricular hypertrophy by renin-angiotensin system blockade. We demonstrate that high cardiac angiotensin II is directly responsible for right and left ventricular hypertrophy. We used transgenic mice overexpressing angiotensinogen in cardiomyocytes characterized by cardiac hypertrophy without fibrosis and normal blood pressure. Angiotensin-converting enzyme inhibition and angiotensin II type 1 receptor blockade prevent or normalize ventricular hypertrophy. Surprisingly, in control mice, receptor blockade decreases tissue angiotensin II despite increased plasma levels. This suggests that angiotensin II may be protected from metabolization by binding to its receptor. Blocking of the angiotensin II type 1 receptor rather than enhanced stimulation of the angiotensin II type 2 receptor may prevent remodeling and account for the beneficial effects of angiotensin antagonists.
Keywords
Angiotensin II, Animals, Blood Pressure, Hypertrophy, Left Ventricular, Hypertrophy, Right Ventricular, Mice, Myocardium
Pubmed
Web of science
Create date
05/03/2008 17:41
Last modification date
20/08/2019 15:05