ALPHA-1-ADRENERGIC STIMULATION OF IODIDE ORGANIFICATION IN MOUSE THYROID INHIBITION BY PROTEIN-KINASE-C INHIBITORS

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, an 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.