Our view of vascular endothelium is in constant evolution. To think of it as the almost inert 'nucleated cellophane' of old is obsolete but even the concept of an active interface between what is inside and what lies outside of blood vessels is becoming hopelessly out of date. Endothelium is not just the customs officer that controls the traffic of small and large molecules or even whole cells across the border, or the frontier police who keep law and order along the vessel walls. It actually moves the frontier line as circumstances require. Endothelium controls local dilatation and narrowing either as a response to or to effect changes in blood flow. It helps building a clot if a lesion needs repairing and overlooks its removal when no longer necessary. It promotes growth of new vessels and dilatation of collaterals when blood is required by ischaemic tissues and diverts blood from existing capillaries, or closes some of them, when not in use.
Endothelium is strategically placed on the vessel wall to: 1) act as a sensor of haemodynamic changes, 2) transduce the signals received by the surrounding cells and matrix, 3) produce mediators influencing growth, activity, migration and death of surrounding cells, and 4) maintain such adaptive changes as they best fit the circulatory requirements [1].
Dilating, closing and opening up of capillaries is precisely what goes on in the diabetic retina and perhaps elsewhere in the diabetic body. Endothelium is likely to play a major role in these remodelling events. Does it simply react to changes in the 'milieu interieur' by intensifying responses that remain otherwise physiological in quality, or do such