All types of clinically employed iodinated roentgen contrast media (CM) cause vasodilatation after i.a. and i.v. administration, regardless of precise molecular structure. It is now apparent, however, that at iodine concentrations which provide equivalent angiographic contrast, this is significantly less with newer hexa-iodinated dimers, such as iodixanol and iotrolan, than older generations of compounds. The cellular mechanisms that underly the vasodilator effects of CM still remain to be fully elucidated but may include a) effects attributable to hyperosmolality; b) stimulation of the release of endogenous vasoactive mediators; and c) direct relaxant effects upon vascular smooth muscle. This review will discuss the possible contributions of these mechanisms to the vasodilatation observed in the clinical situation.