Summary: Canine and human coronary artery rings were studied in organ baths to determine if endothelium-derived relaxing factor (EDRF) modulates the responses to norepinephrine in the same way in both species. In both canine and human preparations, incubated with propranolol (3 μM) and prazosin (1 μM), and contracted with prostaglandin F2α (PGF2α), norepinephrine (0.01-10 μM) induced endothelium-dependent relaxations that were significantly higher in canine preparations than in human preparations (maximal response: 88 ± 5 vs. 32 ± 7%). In another set of experiments, dose-contraction curves were constructed for norepinephrine in the presence of 1 μM propranolol. In both canine and human preparations with intact endothelium, methylene blue (10 μM), an inhibitor of the target enzyme of EDRF, potentiated these dose-contraction curves (ratio in maximal responses: 1.5 ± 0.2 and 2.9 ± 0.2, respectively). NG-monomethyl-l-arginine (l-NMMA) (2 mM), an inhibitor of EDRF formation, also potentiated the norepinephrine-induced contractions. Thus, despite weaker endothelium-dependent relaxations mediated by α2-adrenoceptors in human coronary artery than in canine coronary artery, norepinephrine-induced contractions are modulated by the endothelial function in both species.
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Berkenboom et al. (1991) studied this question.