Bradykinin-Induced, Nω-Nitro-L-Arginine-Insensitive Endothelium-Dependent Relaxation of Porcine Coronary Arteries Is Not Mediated by Bioassayable Relaxing Substances

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Abstract
Summary: The effect of the arginine analogue, Nω-nitro-L-arginine (l-NNA) was studied on bradykinin-induced relaxation in porcine coronary arteries. In the presence of indomethacin (3 × 10−6M) and captopril (10−6M), treatment with l-NNA (10−4M) had no effect on the bradykinin-induced (10−10-10−7M) 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 (10−4M) 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).

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