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Bradykinin‐Induced, N&ohgr;‐Nitro‐L‐Arginine‐Insensitive Endothelium‐Dependent Relaxation of Porcine Coronary Arteries Is Not Mediated by Bioassayable Relaxing Substances

Summary: The effect of the arginine analogue, N&ohgr;‐nitro‐L‐arginine (l‐NNA) was studied on bradykinin‐induced relaxation in porcine coronary arteries. In the presence of indomethacin (3 × 10−6 M) and captopril (10−6 M), treatment with l‐NNA (10−4 M) had no effect on the bradykinin‐induced (10−10‐10−7 M) relaxations in strips contracted with U‐46619. In contrast to the findings in organ chamber experiments, bradykinin‐induced release of endothelium‐derived relaxing factor(s) (EDRFs) was abolished after 45 min of treatment of perfused porcine coronary artery segments with l‐NNA (10−4 M) in a superfusion bioassay system. These results show that, in addition to the release of nitric oxide, endothelium‐dependent relaxation of porcine coronary arteries to bradykinin involves an alternative mechanism(s), which accounts for the relaxation in the presence of l‐NNA. Since the release of a relaxing mediator could not be detected from L‐NNA‐treated porcine coronary artery segments under bioassay conditions, it is postulated that either no diffusible factor(s) is involved in the L‐NNA‐insensitive endothelium‐dependent relaxation, or it is mediated by an extremely labile endothelium‐derived substance(s).