Discrimination by the NO‐trapping agent, carboxy‐PTIO, between NO and the nitrergic transmitter but not between NO and EDRF

Abstract

1. The effects of carboxy-PTIO, a scavenger of free radical nitric oxide (NO), were studied on endothelium-dependent relaxations of rat aorta and nitrergic nerve stimulation-induced relaxations of anococcygeus muscle and gastric fundus strips to test the hypothesis that endothelium-derived relaxing factor (EDRF) and the transmitter released by nitrergic nerves is free radical NO. 2. Carboxy-PTIO (10-300 microM) produced concentration-dependent reductions of relaxations elicited by exogenous NO, and relaxations mediated by EDRF released by acetylcholine and ATP in rings of rat aorta. The inhibitory effect of carboxy-PTIO was removed by washing the tissues. 3. In the rat anococcygeus muscle, carboxy-PTIO (10-300 microM) produced concentration-dependent reductions of relaxations to exogenous NO; however, in concentrations up to 2000 microM it did not reduce relaxations elicited by nitrergic nerve stimulation (1-2 Hz), in fact, concentrations of 300 microM or more slightly enhanced them. 4. In rat gastric fundus strips, carboxy-PTIO (100 and 300 microM) reduced relaxations to exogenous NO, but relaxations elicited by stimulation of the nitrergic component of non-adrenergic, non-cholinergic nerves were not affected. 5. These results suggest that EDRF is free radical NO and may be designated EDNO, but the transmitter released from nitrergic nerves does not appear to be identical to EDNO and may not be free radical NO.