General Introduction

Abstract

Vascular structure is the result of a complex biological enterprise, genetically programmed and controlled. It begins in the embryo with vasculogenesis and continues with angiogenesis. Persistence of a vascular segment throughout life implies biological maintenance. This includes adjustments and renewal of the various components of the segment. Shear stresses are the hemodynamic signals which may induce changes in the vessel wall morphology (remodeling). Such stresses are known to stimulate mainly mural changes and result in focal or regional angioectasia (flow-related aneurysmal formation, development of collateral circulation channels, etc.). Hypertrophic changes in the vessel wall may also result in narrowing of the arterial lumen. Therefore, mural overproduction is evidence of either excessive proliferation or defective apoptosis or both. Shear stresses trigger the vessel wall to remodel in a flexible way, by adjusting or progressively shifting the morphology, rather than creating a new vascular pattern. Conversely, mechanisms of vasculogenesis and angiogenesis (sprouting) require a much greater recruitment of proliferative and apoptotic resources to achieve neovascularization.