Selective over-expression of human ACE1 in the cardiac ventricles of transgenic rats significantly augmented the degree of cardiac hypertrophy after induction of hypertension compared with controls.
Does selective over-expression of human ACE1 in cardiac ventricles augment cardiac hypertrophy following suprarenal aortic banding in rats?
Increased cardiac ACE1 does not spontaneously trigger but augments cardiac hypertrophy in response to pressure overload in a transgenic rat model.
Increased cardiac angiotensin converting enzyme-1 (ACE1) is found in individuals who carry a deletion in intron 16 of ACE1 gene or in individuals who suffer from cardiac disorders, such as hypertrophy. However, whether a single increase in ACE1 expression leads to spontaneous cardiac defects remains unknown. To determine if the increased cardiac ACE1 actively plays a role or is merely the consequence of pathological changes in the process of cardiac hypertrophy, we generated a transgenic rat model with selective over-expression of human ACE1 in the cardiac ventricles. The left ventricular ACE1 activity is elevated about 50-fold in transgenic rats. Angiotensin-1 perfusion of isolated hearts demonstrated a significant decrease in coronary artery flow compared with non-transgenic littermates, suggesting that the transgenic ACE1 is functional. Neither cardiac hypertrophy nor other morphological abnormalities were observed in transgenic rats under standard living conditions. It was found, however, after induction of hypertension by suprarenal aortic banding, that the degree of cardiac hypertrophy in transgenic rats was significantly higher than that of banded control rats. The expressions of both ANF and collagen III, molecular markers of cardiac hypertrophy, were also increased in banded transgenic rats compared with banded control. Our results suggest that increased cardiac ACE1 does not trigger but augments cardiac hypertrophy.
Xiao‐Li Tian (Wed,) conducted a other in Cardiac hypertrophy. Selective over-expression of human ACE1 in cardiac ventricles and suprarenal aortic banding vs. Non-transgenic littermates (banded control rats) was evaluated on Degree of cardiac hypertrophy after induction of hypertension by suprarenal aortic banding. Selective over-expression of human ACE1 in the cardiac ventricles of transgenic rats significantly augmented the degree of cardiac hypertrophy after induction of hypertension compared with controls.