Abstract
Epinephrine was shown to inhibit TSH-stimulated cAMP formation in cat and pig thyroid slices and isolated rat and hamster thyroid lobes. In contrast, no such inhibitory action could be demonstrated in sheep or beef thyroid slices or mouse thyroid-trachea preparations. The inhibitory effect of epinephrine or TSH-stimulated cAMP formation in pig thyroid slices was blocked by 10 .mu.M yohimbine, but not by 10 .mu.M prazosin, suggestive of mediation through an .alpha.2-catecholamine receptor mechanism. In cat thyroid slices, the inhibitory effect of epinephrine was blocked by both yohimbine and prazosin, suggestive of a mixed .alpha.-adrenoceptor mechanism. Meclofenamate and indomethacin attenuated the epinephrine response in cat, but not pig, thyroid slices, but other prostaglandin inhibitors were ineffective. Beef thyroid slices responded to epinephrine with an increase in iodide organification that is mediated through an .alpha.-adrenergic mechanism not blocked by propranolol. This stimulatory effect of epinephrine was abolished by both 10 .mu.M prazosin and 10 .mu.M yohimbine. In contrast to the inhibitory effect of the catecholamines on TSH-stimulated cAMP formation in cats, the stimulatory response of beef iodide organification to epinephrine was not modified by meclofenamate, indomethacin, or verapamil. These findings suggest that the receptor mechanisms mediating the inhibitory effect of catecholamines on cat thyroid and the stimulatory effect of catecholamines in beef thyroid slices may well be mediated by separate and as yet undefined receptor mechanisms. In contrast, the inhibitory effect of epinephrine on TSH-stimulated cAMP formation in pigs is most likely mediated through an .alpha.2-adrenoceptor mechanism. These findings further document the multiplicity of catecholamine actions on thyroid function as well as the diversity observed among various species.
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