Resistance to ACE inhibitors myth or reality?

Angiotensin Converting Enzyme (ACE) inhibitors represent a major advance in the treatment of: hypertension, and generally speaking, in cardiovascular prevention; myocardial infarction; cardiac failure. They have a cardio and vascular protective action by tending to correct hyp ertension, left ventricular hypertrophy and remodelling, endothelial dysfun ction, arterial smooth muscle proliferation and thrombotic phenomena. Howev er, besides the cough that this therapeutic class engenders, a major questi on remains unanswered : is there resistance to this family of drugs? In oth er words, does left ventricular remodelling and arterial smooth muscle prol iferation continue with regular treatment at the prescribed dosages? The sy nthesis of angiotensin II does not only depend on the angiotensin convertin g enzyme but also on the quality of angiotensin I and the presence of other enzymes such as chymase. A secondary increase of angiotensin II with ACE i nhibitor therapy may reflect insufficient blockade of the renin-angiotensin system or a synthesis of angiotensin II by an alternative pathway to the c onverting enzyme. In vivo measurement of ACE inhibition shows that blockade of the renin-angi otensin system is automatically limited due to the very accurate regulation of angiotensin II concentrations.