Direct Actions of AT ₁ (Type 1 Angiotensin) Receptors in Cardiomyocytes Do Not Contribute to Cardiac Hypertrophy

Activation of AT 1 (type Ang) receptors stimulates cardiomyocyte hypertrophy in vitro. Accordingly, it has been suggested that regression cardiac associated with renin-Ang system blockade is due to inhibition cellular actions Ang II the heart, above and beyond their effects reduce pressure overload. We generated 2 distinct mouse lines cell-specific deletion 1A receptors, from cardiomyocytes. In first line (C-SMKO), elimination was achieved using a heterologous Cre recombinase transgene under control Sm22 promoter, which expresses cells smooth muscle lineage including cardiomyocytes vascular conduit but not resistance vessels. The second (R-SMKO) utilized knocked-in locus, drives expression myocytes both arteries. Thus, although groups lack cardiomyocytes, they are distinguished by presence (C-SMKO) or absence peripheral responses II. Similar wild-types, chronic infusion caused hypertension C-SMKO mice, whereas were reduced R-SMKOs. despite C-SMKOs develop robust hypertrophy. By contrast, R-SMKOs developed identical levels response overload–induced transverse aortic banding. Our findings suggest direct activation minimal influence on induced