In hypertension, the thickening of the arterial wall by an increase in the cellular mass and collagen and elastin content may be considered to be an adaptive response to the high blood pressure. Positive and negative feedback systems play a role in the hypertension-vascular hypertrophy couple. Increased wall stress associated with stretching of the smooth muscle acts as a mechanical agonist of cellular growth in synergy with plasma or autocrine growth factors. In general, vascular hypertrophy ceases when the stress returns to normal. However, the increase in cell mass may result in an increase in systemic vascular resistance due to muscular hypertonicity and lead to an amplification of the hypertensive condition. The mechanisms of mechano-transduction are not fully understood. Moreover, genetic vascular changes affecting the structure of the vessels, the sensitivity to vasoactive substances or the geometry of the vascular system can also induce hypertension.