Angiotensin converting enzyme (ACE) inhibitors induce haemodynamic, humoral and metabolic actions which have been well characterized during the last decade. The precise mechanisms involved in these actions still need clarification. Among the many questions we need answered are the following: under steady-state conditions, does plasma ACE activity reflect angiotensin I conversion in tissues? Do the low levels of angiotensin II observed after ACE inhibition still contribute to vascular tone? What is the precise role of extrarenal tissue renin in the regulation of vascular tone? What is the role of bradykinin, prostaglandins and the interaction with the sympathetic nervous system in the antihypertensive effect of ACE inhibition? We hope that definite answers to these questions will be found during the second decade of the use of ACE inhibitors.