Is circulating noradrenaline the cause of varicose veins?

When noradrenaline, either endogenous or exogenous, is released from the venae venarum of a dog's lateral saphenous vein which is constricted by noradrenaline, it dilates the vein. By limiting the release of the drug to just a section of the vein's venae venarum network it is possible to dilate the normal vein segmentally, that is, cause varicosities. This has led to the suggestion that pathological varicosities begin as localised physiological dilator responses of the vein wall to circulating endogenous noradrenaline, released from the vein's venae venarum. Under ambulatory conditions small quantities of noradrenaline probably flow almost continually from the lumen of the vein to different parts of its venae venarum network and serve to adjust constrictor tone downwards. When there is turbulence in the vein lumen the volume of reflux becomes excessive and causes so much adjustment that constrictor tone is abolished. The vein, in effect, then exhibits a frank dilator effect, visible as a varicosity, localised to the level in the vein at which the turbulence occurs. If a high volume of hypoxic blood reflux continues for a critical period then the wall of the varicosity suffers secondary degenerative structural changes which make the varicosity permanent.