Effects of prostaglandins Fα on dog thyroid cyclic AMP level and function |
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Authors: | J Van Sande P Cochaux C Decoster JM Boeynaems JE Dumont |
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Institution: | Institute of Interdisciplinary Research, Erasmus Hospital, Bât. C, Route de Lennick 808, 1070 Brussels Belgium |
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Abstract: | Prostaglandins F1α and F2α, at high concentrations (≥28 μM) enhanced cyclic AMP accumulation in dog thyroid slices. At lower concentrations, they inhibited the cyclic AMP accumulation induced by thyrotropin (TSH), prostaglandin E1, and cholera toxin. This effect was rapid in onset and of short duration, calcium-dependent and suppressed by methylxanthines. Prostaglandin Fα also inhibited TSH-induced secretion and activated iodine binding to proteins. These characteristics are similar to those of carbamylcholine action, except that prostaglandins F did not enhance cyclic GMP accumulation. The effect of prostaglandin Fα was not inhibited by atropine, phentolamine and adenosine deaminase and can therefore not be ascribed to an induced secretion of acetylcholine, norepinephrine or adenosine. It is suggested that prostaglandins F act by increasing influx of extracellular Ca2+. Arachidonic acid also inhibited the TSH-induced cyclic AMP accumulation. However this effect was specific for TSH, it was enhanced in the absence of calcium and was not inhibited by methylxanthines or by indomethacin at concentrations which completely block its conversion to prostaglandin Fα. Arachidonic acid action is sustained. This suggests that arachidonic acid inhibits thyroid adenylate cyclase at the level of its TSH receptor and that this effect is not mediated by prostaglandin Fα or any other cyclooxygenase product. |
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Keywords: | Cyclic AMP (Dog thyroid) TSH thyroid stimulating hormone IBMX isobutylmethylxanthine EGTA |
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