Inhibition of the angiotensin converting enzyme (ACE) results in suppression of the formation of angiotensin II and delay of the degradation of bradykinin. Hence, the pharmacological effects of ACE inhibitors are attributable to both of these mechanisms. This is a brief review of the haemodynamic, neurohumoral and metabolic alterations following ACE inhibition, with an attempt to separate those attributable to the angiotensin-mediated actions and those attributable to bradykinin-mediated actions as they relate to prevention or attenuation of cardiac damage in hypertension, myocardial ischaemia and congestive heart failure.