Many aspects of vascular caliber can be accounted for on the basis of interactions between the frictional drag generated by the stream, and the sensitivity of the endothelial cells to this force. When the drag force on endothelial cells is at its critical set-point, these lining cells are at rest with respect to factors that affect caliber. An increase in flow rate increases the drag and appears to induce the endothelium to generate a signal that triggers relaxation of the subjacent medial smooth muscle. The resulting functional dilatation of the vessel reduces the stream velocity and returns the drag to its set-point. If the drag stimulus is persistent or recurrent, vasodilatation is soon followed by anatomical reorganization of the vessel around its enlarged lumen. This sequence can account for gradual, generalized and regional vascular growth, and for the opening of collateral vessels. This sequence may also play a role in the enlargement of veins, lymphatics, airways and other vessels. Turbulence greatly increases drag per unit volume of flow. Aneurysms and and post-stenotic dilatations are considered to result from an increased drag. Jets increase drag to an even greater extent and may account for saccular aneurysms and for ‘jet lesions’. Conversely, reduced flow diminishes drag and thereby triggers constriction of the vascular smooth muscle. Persistent reduction of drag permits proliferation of the subendothelial connective tissue, which reduces vascular caliber until the drag on the lining cells is returned to its set-point. Progressive localized narrowings (stenoses) may also be attributed to a reduced drag. Thus high velocity flow around an irregularity such as a plaque may separate the streamlines from the wall at the downstream end of the narrowing. In this region of separation the cells respond to the reduced local flow and drag by subendothelial proliferation and ingrowth, producing further narrowing. These mechanisms may be operative in