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