Key result
EDRF release in human isolated coronary arteries is poorly antagonized by nitric oxide synthase inhibitors L-NOARG and L-NMMA, suggesting an alternative pathway or additional relaxing factors.
Nitric oxide synthase inhibitors poorly antagonize EDRF-mediated relaxation in human coronary arteries, suggesting alternative transduction pathways or the involvement of endothelium-derived hyperpolarizing factor.
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Questions NOS inhibitor utility in human coronary studies; leaves open alternative EDRF pathways for targeted investigation.
Stork et al. (1994) studied Cardiac transplant patients (tissue source). EDRF-releasing agents (substance P, bradykinin, histamine, A23187, ionomycin) vs. Nitric oxide synthase inhibitors (L-NOARG, L-NMMA) or endothelium removal was evaluated on Relaxation responses. EDRF release in human isolated coronary arteries is poorly antagonized by nitric oxide synthase inhibitors L-NOARG and L-NMMA, suggesting an alternative pathway or additional relaxing factors.
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