Despite a well-established rationale for pharmacologically induced arterial and venous vasodilatation in congestive heart failure, the clinical usefulness of long-term vasodilator therapy without concomitant converting-enzyme inhibition generally has been disappointing. With the exception of nitrates and, possibly, the combination of nitrates and hydralazine, the use of converting-enzyme inhibitors in many aspects appears preferable in the majority of patients. This article reviews the pathophysiology of inappropriate vasoconstriction in heart failure, the cellular mode of action of the various vasodilators, hemodynamic effects with respect to the peripheral site of action, clinical usefulness and limitations of different vasodilators, and the various determinants of clinical efficacy. Finally, an attempt is made to assess when and how to introduce vasodilator treatment with and without concomitant ACE inhibition.