| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Endocrinology, Vol 110, 1023-1029, Copyright © 1982 by Endocrine Society
ARTICLES |
K Mashita, S Kawamura, B Kishino, H Kimura, K Nonaka and S Tarui
We have established a perifusion system using rat thyroid. With this system, we analyzed the effects of TSH, 3-isobutyl-1-methylxanthine (IBMX) and iodide on the release of T3 and of cAMP, paying special attention to the relation between the release of the two substances. During perifusion, which was continued for 7 h, T3 release increased progressively with time and in a dose-related manner when TSH was added at concentrations of 0.1-10 mU/ml. However, cAMP release was unappreciable even in the presence of 10 mU/ml TSH. The release of T3 and cAMP was markedly enhanced by 3 x 10(-4) M IBMX. When iodide was added, a marked increase in cAMP release was unexpectedly observed. However, a slight but significant suppression of TSH-stimulated T3 release was shown with 1 x 10(-3) M iodide. TSH-stimulated T3 release was almost completely inhibited by 1 x 10(-3) M 6-n-propyl-2- thiouracil, but such a complete inhibition did not occur with 2- mercapto-1-methylimidazole. The cAMP release stimulated by IBMX was not affected by 6-n-propyl-2-thiouracil, but that stimulated by iodide was effectively inhibited. The present studies indicate that TSH and IBMX enhance T3 release, but only IBMX increases cAMP release. Iodide also results in a marked increase in cAMP release but does not affect T3 release from unstimulated thyroid and inhibits T3 release from TSH- stimulated thyroid. We suggest that there is not necessarily any close correlation between T3 release and cAMP release into perifusates of the rat thyroid.
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |