Ventricular hypertrophy following chronic overload results from the hypertrophy of cardiomyocytes and the hyperplasia of non muscle cells in the heart. The mechanisms by which hemodynamic stress induces these cellular adaptations are unknown. However, an increasing body of evidence seems to favor local paracrine and/or autocrine mechanisms rather than circulating factors. Locally, it is well established that cardiac endothelium regulates myocardial contraction by the release of nitric oxide, prostacyclin, endothelin and other still unidentified factors. Similarly, endothelial factors seem involved in myocyte growth alteration, especially those occurring around coronary vessels, at the early stage of hemodynamic stresses. This involves factors such as endothelin and angiotensin II that are known to induce changes in both cardiac myocyte and non muscle cell growth. On the other hand, an autocrine function of myocardial cells has also been proposed. Mechanical stress provokes the release of cardiomyocyte-derived growth factors, including Fibroblast Growth Factors, that may induce angiogenesis and proliferation and survival of many cell types. Thus, in the heart, cardiomyocytes and non muscle cells sense acute mechanical stretch and exert paracrine and/or autocrine regulation of their growth.