Alpha 1-adrenergic stimulation of iodide organification in mouse thyroid--inhibition by protein kinase C inhibitors
Muraki, T.; Tsukahara, F.; Fujii, E.; Nomoto, T.
Archives Internationales de Pharmacodynamie et de Therapie 314: 122-132
1991
ISSN/ISBN: 0003-9780 PMID: 1688097 Document Number: 379996
Using mouse thyroid lobes incubated in vitro, a study was made of the subtype of alpha-adrenoceptors involved in iodide organification, induced by norepinephrine, and the possible role of protein kinase C in mediating the effect of norepinephrine. Norepinephrine and phenylephrine, alpha 1-agonists, increased the iodide organification in mouse thyroid lobes; however, clonidine, and alpha 2-agonist, showed a marginal effect. Prazosin, an alpha 1-blocker, but not yohimbine, an alpha 2-blocker, inhibited the norepinephrine-induced iodide organification. These results suggest the involvement of alpha 1-adrenoceptors. The stimulation of the iodide organification, induced by norepinephrine, was inhibited by omission of calcium from the medium and by protein kinase C inhibitors such as H 7, quercetin and trifluoperazine, but not by W-7, a calmodulin antagonist. Since tetradecanoylphorbol acetate, a stimulator of protein kinase C, mimicked the effect of norepinephrine in increasing iodide organification, extracellular calcium ion and protein kinase C would appear essential to the alpha 1-adrenergically regulated iodide organification in mouse thyroid.