Prostacyclin induces a surprising long-lasting motility in quiescent uterine strips (indomethacin-treated) isolated from ovariectomized rats
Dose-response curves for several prostaglandins (PGI2; PGD2; PGF2 and PGE2); BaCl2 or prostaglandin metabolites (15-keto-PGF2α; 13, 14-diOH-15-keto-PGF2α; 6-keto-PGF1α and 6-keto-PGE1 in quiescent (indomethacin-treated) uterine strips from ovariectomized rats, were constructed. All PGs tested as wel...
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1983
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00906980_v26_n4_p663_Gimeno http://hdl.handle.net/20.500.12110/paper_00906980_v26_n4_p663_Gimeno |
| Aporte de: |
| Sumario: | Dose-response curves for several prostaglandins (PGI2; PGD2; PGF2 and PGE2); BaCl2 or prostaglandin metabolites (15-keto-PGF2α; 13, 14-diOH-15-keto-PGF2α; 6-keto-PGF1α and 6-keto-PGE1 in quiescent (indomethacin-treated) uterine strips from ovariectomized rats, were constructed. All PGs tested as well as BaCl2, triggered at different concentrations, evident phasic contractions. Within the range of concentrations tested the portion of the curves for the metabolites of PGF2α was shifted to the right of that for PGF2α itself; the curve for 6-keto-PGF1α was displaced to the right of the curve for PGI2 and that for 6-keto-PGE1 to the left. It was also demonstrated that the uterine motility elicited by 10-5 M PGF2α and its metabolites was long lasting (more than 3 hours) and so it was the activity evoked by PGI2; 6-keto-PGF1α and BaCl2, but not the contractions following 6-keto-PGE1, which disappeared much earlier. The contractile tension after PGF2α; 15-keto-PGF2α; 13, 14-diOH-15-keto-PGF2α and PGI2, increased as time progressed whilst that evoked by 6-keto-PGF2α or BaCl2 fluctuated during the same period around more constant levels. The surprising sustained and gradually increasing contractile activity after a single dose of an unstable prostaglandin such as PGI2, on the isolated rat uterus rendered quiescent by indomethacin, is discussed in terms of an effect associated to its transformation into more stable metabolites (6-keto-PGF1α, or another not tested) or as a consequence of a factor which might protects prostacyclin from inactivation. © 1983. |
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