Captopril increased mitochondrial coenzyme Q10 level, improved respiratory chain function and energy production in the left ventricle in rabbits with smoke mitochondrial cardiomyopathy

The aim of the study was to show whether the ACE inhibitor captopril is able to protect the heart against the deleterious effect of passive cigarette smoking on left ventricular mitochondria. Four groups of rabbits were investigated: control (C), passive smoking of three cigarettes twice daily/30 minutes (S), control + captopril (7.5 mg/kg body weight twice daily) (Cap), and smoking + captopril (SCap) as in group 2 and 3. Three weeks lasting passive smoking impaired oxidative phosphorylation, diminished cytochrome oxidase activity and increased the mitochondrial Fr-ATPase protein concentration. Moreover, the level of coenzyme Q(10) (CoQ(10)) and coenzyme Q(9), were decreased. Simultaneous treatment with captopril prevented partly the decrease of CoQ(10) level, deterioration of oxidative phosphorylation, diminution of cytochrome oxidase activity and enhancement of F-1-ATPase level. We conclude that captopril protected the myocardium against the harmful effect of passive smoking in rabbits.