Boeynaems J M, Waelbroeck M, Dumont J E
Endocrinology. 1979 Oct;105(4):988-95. doi: 10.1210/endo-105-4-988.
Dog thyroid slices released in their incubation medium prostaglandins E2 (PGE2), F2 alpha (PGF2 alpha), 15-keto-13,14-dihydro-F2 alpha, and thromboxane B2 (TxB2), as measured by direct RIA. This release could be inhibited by indomethacin and naproxen, indicating that it corresponded to a neosynthesis. Carbamylcholine (2--100 microns) stimulated the release of PGE2, PGF2 alpha, and TxB2, whereas epinephrine (20 microns to 1 nM) enhanced the release of PGE2 and PGF2 alpha but had no effect on TxB2. These stimulations were inhibited by atropine and dihydroergocryptine, respectively, suggesting that a muscarinic and an alpha-adrenergic receptor were involved. The ionophore A23187 reproduced these stimulations, and the stimulatory effects of carbamylcholine and epinephrine were inhibited in the absence of exogenous Ca++ and after EGTA depletion. Ca++ thus appears as a major regulator of PG production in the thyroid. TSH (0.06--10 MU/ml) and dibutyryl cAMP had no effect on the release of PGE2, PGF2 alpha, or TxB2 by dog thyroid in vitro.
