Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.6.1.2 (guanylate cyclase)
 8,497 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the effect of fentanyl on the endothelium-dependent vascular responses in isolated rat aortic strips. Fentanyl depressed the endothelium-dependent relaxation induced by acetylcholine but not that induced by the calcium ionophore, A23187. Endothelium-independent relaxation in response to sodium nitroprusside (SNP), a soluble guanylate cyclase activator, was not depressed by fentanyl. On the other hand, fentanyl depressed the increase in cyclic GMP level stimulated by acetylcholine but not that stimulated by A23187 or SNP. Furthermore, fentanyl depressed the vasocontraction by acetylcholine but not that by histamine or KCl in isolated pig coronary artery strips without endothelium, suggesting that fentanyl can inhibit endothelium-independent contraction via muscarinic receptor on smooth muscle cells. These results suggest that fentanyl can inhibit endothelium-dependent vasorelaxation via endothelium-derived relaxing factor (EDRF) by acting on endothelial cells but not on smooth muscle cells. The inhibitory effect of fentanyl on the relaxation probably occurs at the level of muscarinic receptor on endothelial cells or at a site before biochemical pathways converting L-arginine to EDRF.
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PMID:[Inhibitory effect of fentanyl citrate on endothelium-dependent relaxation in rat aorta]. 830 61