QUINAPRIL IS DEESTERIFIED TO THE PRINCIPAL METABOLITE, QUINAPRILAT, WHICH IS AN INHIBITOR OF ACE ACTIVITY IN HUMAN SUBJECTS AND ANIMALS. ACE IS A PEPTIDYL DIPEPTIDASE THAT CATALYZES THE CONVERSION OF ANGIOTENSIN I TO THE VASOCONSTRICTOR, ANGIOTENSIN II. THE EFFECT OF QUINAPRIL IN HYPERTENSION AND IN CONGESTIVE HEART FAILURE (CHF) APPEARS TO RESULT PRIMARILY FROM THE INHIBITION OF CIRCULATING AND TISSUE ACE ACTIVITY, THEREBY REDUCING ANGIOTENSIN II FORMATION. QUINAPRIL INHIBITS THE ELEVATION IN BLOOD PRESSURE CAUSED BY INTRAVENOUSLY ADMINISTERED ANGIOTENSIN I, BUT HAS NO EFFECT ON THE PRESSOR RESPONSE TO ANGIOTENSIN II, NOREPINEPHRINE OR EPINEPHRINE. QUINAPRIL INCREAES IN LAG TIME TO OXIDATION OF LDL BY 48%, CAUSES 35% INCREASE IN ERYTHROCYTE SUPEROXIDE DISMUTASE ACTIVITY ( SUPEROXIDE DISMUTASE STABILISES REACTIVE OXYGEN SPECIES-ROS & INCREAES NO) & 20% REDUCTION IN 8-ISOPROSTANE LEVELS ( A CLINICAL MARKER OF OXIDATIVE STRESS). THUS QUINAPRIL IS BENEFICIAL IN THE PREVENTION OF ATHEROSCLEROSIS IN PATIENTS WITH METABOLIC SYNDROEM. IT IMPROVES SYMPATHETIC TO PARASYMPATHETIC RATIO, THUS PROVIDING BENEFITS IN DIABETIC AUTONOMIC NEUROPATHY. IT REDUCES ALBUMIN EXCRETION RATE IN 90% PATIENTS WITH PROTEINURIA PROVIDING RENOPROTECTION.