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Endogenously produced nitric oxide (NO) induces relaxation in smooth muscle in various organs. The purpose of this study was to investigate whether a NO-mediated relaxation system exists in the human Fallopian tube. To study contractility, the isthmic portion of the tube was obtained from 23 fertile women during operations due to benign non-tubal diseases. Tubal smooth muscle strips were mounted in tissue chambers containing HEPES buffer and connected to a Grass transducer for the isometric registration of contractile activity. By adding L-arginine (the substrate for NO synthesis) or N-nitro-L-arginine methyl ester (L-NAME; an inhibitor of NO synthesis) to the tissue chambers, changes in tubal contractility were monitored. The addition of L-NAME caused increased tubal contractility, while L-arginine, after an initial transient increase in tonus, caused relaxation of the strips. Using immunohistochemistry, NO synthase, the enzyme that catalyses the production of NO from L-arginine, was identified in tubal tissue cells. These results indicate that a NO-dependent relaxation system exists in the Fallopian tube and that NO may play a role as a mediator of tubal contractility.

Evidence for nitric oxide mediation of contractile activity in isolated strips of the human Fallopian tube