Our systemic arteries branch from the large aorta to increasingly smaller vessels, ending in the capillary bed that allows perfusion and oxygenation of all tissue in the body. This is an amazingly large network, containing hundreds of millions of blood vessel segments. Their diameter varies from 25 mm in the aorta to 0.01 mm in the most distal segments. In order to maintain blood flow through this network, a driving pressure is needed, which is the blood pressure generated by the heart. The ratio of pressure and flow is the resistance of this network. It turns out that vessels of around 0.2 mm and smaller contribute to this resistance. Hence these vessels are called resistance arteries or small arteries. You cannot easily see them (on MRI or CT) or feel them (from the pulse). Yet they are there and they form the very vast majority of the arterial segments. The small arteries have a very important task: to regulate local blood flow in each and every corner of our body. They do so by adjustments of their diameter. Quick functional changes are accomplished by contraction and relaxation of smooth muscle cells in the wall. Chronic changes in diameter result from reshaping of the vascular wall, where existing elements are reorganized, new elements are added or elements are broken down. We call this vascular remodeling. The regulation of arterial diameter and wall structure is a continuous process of adaptation to changing needs, ranging from exercise to development of the body. This adaptation may malfunction: too small a diameter of the resistance vessels relates to insufficient tissue perfusion as well as hypertension. The vascular wall consists of amongst others the vascular smooth muscle cells, endothelial cells that line the lumen, and elastic fibers and other extracellular matrix elements. Physical forces form an important part of the adaptation mechanisms of small arteries: Blood pressure causes distension of the matrix elements, but also induces contraction of the smooth muscle cells and production of more cells and more matrix. Blood flow is sensed by the endothelial cells, which release factors such as nitric oxide that cause relaxation and remodeling towards larger diameters. Forces, cells and matrix therefore form a triangle of mutual effects that underlie vascular adaptation. We aim to unravel the functioning of this triangle.