Decreased endothelin binding and receptor density in varicose veins

Abstract

Abstract Background The primary cause of venodilatation and reduced contractility in varicose veins is unclear. Endothelin (ET) 1 acts on smooth muscle cell ET A/ET B receptors to induce contraction and growth, and on endothelial cells to induce production of the vasorelaxant and growth inhibitors nitric oxide and prostacyclin. These factors may be involved in the aetiology of varicose veins. This study investigated ET-1 binding and ET A/ET B receptor density in varicose and non-varicose veins. Methods Proximal long sapheous vein (LSV) sections from nine patients undergoing surgery for varicose veins were compared with normal LSV from nine patients undergoing coronary artery bypass surgery. Slide-mounted sections were incubated in [125I]-radiolabelled ET-1 and ET A/ET B binding sites were identified using subtype-selective radioligands. Receptor density and distribution was quantified on autoradiographs by densitometry and binding was localized at the cellular level by nuclear emulsion. Results ET-1 binding and ET B receptor density decreased significantly in the varicose group. There was no significant difference in ET A receptor density. Conclusion Decreased ET-1 binding may contribute to venodilatation and poor contractility in varicose veins. This may be due to decreased tunica media ET B receptor density.