Effect of Thyroid-stimulating Hormone and Prostaglandins on Thyroid Adenyl Cyclase Activation and Cyclic Adenosine 3',5'-Monophosphate

Abstract

Abstract Thyroid-stimulating hormone (TSH) increased within 1 min the adenyl cyclase activity of bovine and canine thyroid homogenate. A similar effect was also found when adenyl cyclase activity was measured in thyroid slices. In experiments in vivo, adenyl cyclase activity was augmented within 3 min after TSH injection, but this effect did not persist for 60 min after the injection. Despite the transient stimulation of adenyl cyclase activity, increased 14C-1-glucose oxidation was still present 60 min after TSH injection. Stimulation in vitro of adenyl cyclase activity in thyroid homogenate was obtained using as little as 1 milliunit of TSH while adrenocorticotropic hormone and prolactin were without effect. TSH did not increase adenyl cyclase activity in adrenal or testis homogenates. TSH stimulation could still be obtained in the presence of 10-2 m NaF. TSH did not modify thyroid phosphodiesterase activity under conditions in which it stimulated adenyl cyclase activity. TSH rapidly increased cyclic adenosine 3',5'-monophosphate (cyclic AMP) concentration in canine thyroid slices while luteinizing hormone, adrenocorticotropic hormone, and prolactin were ineffective. Although NaF stimulated adenyl cyclase activity and 14C-1-glucose oxidation in canine thyroid slices, it did not increase cyclic AMP concentrations. During 15-min incubations, 10-2 m theophylline had very little effect on cyclic AMP levels, but significantly increased them during 2-hour incubations. At both times, the effect of TSH on cyclic AMP was markedly potentiated by theophylline. Prostaglandin E2 reproduced effects of TSH on both 14C-1-glucose oxidation and cyclic AMP concentration in canine thyroid slices. Prostaglandin F1α stimulated 14C-1-glucose oxidation, but did not increase cyclic AMP levels. Prostaglandin B1 did not modify either cyclic AMP concentrations or 14C-1-glucose oxidation.