Transgenic mice overexpressing the rat angiotensinogen gene in the heart developed myocardial hypertrophy without fibrosis independently of hypertension, showing local Ang II mediates hypertrophy.
Cardiac hypertrophy is frequent in chronic hypertension. The renin-angiotensin system, via its effector angiotensin II (Ang II), regulates blood pressure and participates in sustaining hypertension. In addition, a growing body of evidence indicates that Ang II acts also as a growth factor. However, it is still a matter of debate whether the trophic effect of Ang II can trigger cardiac hypertrophy in the absence of elevated blood pressure. To address this question, transgenic mice overexpressing the rat angiotensinogen gene, specifically in the heart, were generated to increase the local activity of the renin-angiotensin system and therefore Ang II production. These mice develop myocardial hypertrophy without signs of fibrosis independently from the presence of hypertension, demonstrating that local Ang II production is important in mediating the hypertrophic response in vivo.
Mazzolai et al. (Mon,) conducted a other in Cardiac hypertrophy. Overexpression of rat angiotensinogen gene in the heart was evaluated on Myocardial hypertrophy. Transgenic mice overexpressing the rat angiotensinogen gene in the heart developed myocardial hypertrophy without fibrosis independently of hypertension, showing local Ang II mediates hypertrophy.