Angiotensin II Partly Mediates Mechanical Stress–Induced Cardiac Hypertrophy

摘要: We have previously shown that mechanical stress induces activation of protein kinases and increases in specific gene expression synthesis cardiac myocytes, all which are similar to those evoked by humoral factors such as growth hormones. Many lines evidence suggested angiotensin II (Ang II) plays a vital role hypertrophy, it has been reported secretion Ang from cultured myocytes was induced stretch. To examine the stress-induced we stretched neonatal rat absence or presence receptor antagonists saralasin (an antagonist both type 1 2 receptors), CV-11974 (a receptor-specific antagonist), PD123319 antagonist). Stretching 20% using deformable silicone dishes rapidly increased activities mitogen-activated (MAP) kinase activators MAP kinases. Both partially inhibited stretch-induced kinases, whereas showed no inhibitory effects. amino acid incorporation, also approximately 70% with pretreatment CV-11974. When culture medium conditioned stretching cardiocytes transferred nonstretched increase activity observed, this completely suppressed These results suggest an important hypertrophy there other (possibly nonsecretory) induce hypertrophic responses.