학술논문
Pressure-overload hypertrophy is unabated in mice devoid of AT1A receptors.
Document Type
Article
Author
Source
Subject
*CARDIAC hypertrophy
*PHYSIOLOGY
*
Language
ISSN
0363-6135
Abstract
Studies the role of renin-angiotensin system (RAS) in regulating cardiac hypertrophy in response to a hemodynamic overload. Examination on the left ventricular hypertrophic response to a pressure overload in mice devoid of the AT1A receptor; Involvement of multiple mechanisms in cardiac hypertrophic process; Putative major effector of the growth response of the RAS.