The effect of captopril on nitric oxide formation and on generation of radical forms of mitochondrial respiratory chain compounds in ischemic rat heart

The increase of radical forms of mitochondrial respiratory chain compounds (MRCC) is an indicator of an increased risk of the formation of oxygen radi cals. Using electron paramagnetic resonance (EPR), we found an increase of signals corresponding to ubisemichinone radical (. QH) and ironsulfur prote ins radical forms (. FeS) of these respiratory chain compounds during ische mia in the isolated perfused rat heart (. QH increased from 1.51 to 3.08, F eS1 from 1.14 to 2.65 arbitrary units). During the 5-min reperfusion, the s ignals returned to normoxic levels. In isolated mitochondria exposed to ano xia and reoxygenation the radical forms of . QH and . FeS2 changed in a sim ilar manner as in the intact heart. A combination of in vivo captopril trea tment and in vitro L-arginine administration significantly decreased the le vels of MRCC radicals in the isolated myocardium (. QH from 2.61 to 1.72 an d . FeS1 from 1.82 to 0.46 under normoxia; . QH from 4.35 to 2.66 and . FeS 1 from 1.93 to 1.35 during ischemia). This decrease in MRCC radical forms w as associated with increased NO levels in the perfusate, determined as NO2- /NO3-, as well as tissue NO levels determined using EPR as the dinitrosyl i ron complex (DNIC). These results provide new information about the cardiop rotective effects of ACE inhibitors and L-arginine.