The venous valve agger and plasma noradrenaline-mediated venodilator feedback

Abstract

Objective: To investigate the structure and function of the venous valve agger, a fibroelastic structure located at the base of every valve in veins that are responsive to noradrenaline (NA). Design: Constant flow perfusion studies of the responses of in situ and in vitro canine lateral saphenous vein segments to NA and electrical stimulation, supplemented by histological studies of the segments. Setting: University Departments of Physiology and Histology. Materials: Segments of canine lateral saphenous vein. In vitro = 84, in situ = 60 plus. Results: The agger is a crescentic fibroelastic sleeve, spanning the vein wall very obliquely through which the local vasa venarum network drains. It has a dedicated musculature which, when the tone rises, contracts and stretches the fibroelastic of the agger and opens the drainage channels to reflux. Each agger has four muscles, two each of which insert on the concave and convex margins of the agger. They pull in opposite directions when they contract. Conclusions: The agger forms part of a complex that, in conjunction with its dedicated musculature, a reversible transmural pressure gradient and physiological turbulence in the valve sinuses, positively facilitates drainage from the local segment of the vasa venarum network when venous tone is normal; and when venous tone is elevated it pumps and sucks blood from the lumen of the vein to perfuse the vasa venarum network. When the plasma NA in the perfusate diffuses from the network, it causes a localized venodilator feedback effect that restores the elevated tone of the vein to normal. The feedback effect is potent, being estimated to reduce the venonstrictor effect of neuronal NA by about 50% when flow is laminar and considerably more when flow is turbulent. There is evidence that plasma NA may constitute the lateral inhibitory component of the NA chemostimulus of the smooth muscle cell, neuronal NA constituting the excitor component. A chronic breakdown in agger function is believed to be the cause of varicose veins.