Mechanism of the production of reactive nitrogen species during renal ischemic-reperfusion insult

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In circulation, nitric oxide(NO) exists as relatively atable hemoglobin-NO adduct(HbNO), which means that the amount of HbNO may reflect the blood NO concentration. HbNO signal has been reported to be successfully detected in human blood using electron paramagnetic resonance(EPR) method. However, there were some difficulties to obtain a fine HbNO signal of nornal blood. We itroduced the EPR signal subtraction method to overcome the difficulties. Using this method, we confirmed that HbNO concentrarion in pentobarbital-anesthetized rats were augmented by infusion of L-arginine but not D-argimine. We also emenstrated that temocapril, an ACE inhibitor, improved abnormalities of NO dynamics in the L-MAME-induced hypertensive rats.After the intravebous infusion of ^<15>NO_2, the left renal artery of a rat was clumped for 40 minutes. Five minutes after the release of left renal occluaion, left and right renal tissues and venous blood were obtained. Hb^<15>NO concentration of renal tissues and venous blood was evaluated using EPR method. Hb^<15>NO concentrarion of left (ischemic) renal tissue is much higher than that of right(non-ischemic) renal tissue. Hb^<15>NO concentration of venous blood in ischemic-reperfused rat is much higher than that in aham operated non-ischemic rat. These results indicate that there is NO generation pathway from NO_2 and ischemic-reperfusion insult stimulates the NO generation from NO_2