1987Journal of EndocrinologyRequires access

Alpha1-adrenoceptor production of inositol phosphates mediates the inhibition of thyroxine release from the mouse thyroid

Takamura Muraki, Toshio Nakaki, R Kato

Open publisher page 6 citations

Abstract

To examine the mechanism of the alpha 1-adrenoceptor-mediated inhibition of the release of thyroid hormones in the mouse thyroid, the effect of noradrenaline on the production of inositol phosphates was investigated using thyroids preloaded with [3H]inositol. Noradrenaline increased [3H]inositol accumulation into inositol phosphates in the mouse thyroid during a 30-min incubation whereas TSH (10 mU/ml) was without effect. The effect of noradrenaline was mimicked by phenylephrine, but not by clonidine or isoprenaline. Prazosin antagonized the effect of noradrenaline, while yohimbine had no effect. These results suggest that noradrenaline-induced production of inositol phosphates is mediated by alpha 1-adrenoceptors. The inhibition of release of thyroid hormones elicited by alpha 1-adrenergic agonists in the mouse thyroid is possibly mediated through the hydrolysis of membrane phosphoinositides followed by the generation of second messengers such as inositol phosphates and diacylglycerol.

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To examine the mechanism of the alpha 1-adrenoceptor-mediated inhibition of the release of thyroid hormones in the mouse thyroid, the effect of noradrenaline on the production of inositol phosphates was investigated using thyroids preloaded with [3H]inositol. Noradrenaline increased [3H]inositol accumulation into inositol phosphates in the mouse thyroid during a 30-min incubation whereas TSH (10 mU/ml) was without effect. The effect of noradrenaline was mimicked by phenylephrine, but not by clonidine or isoprenaline. Prazosin antagonized the effect of noradrenaline, while yohimbine had no effect. These results suggest that noradrenaline-induced production of inositol phosphates is mediated by alpha 1-adrenoceptors. The inhibition of release of thyroid hormones elicited by alpha 1-adrenergic agonists in the mouse thyroid is possibly mediated through the hydrolysis of membrane phosphoinositides followed by the generation of second messengers such as inositol phosphates and diacylglycerol.

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Available abstract

To examine the mechanism of the alpha 1-adrenoceptor-mediated inhibition of the release of thyroid hormones in the mouse thyroid, the effect of noradrenaline on the production of inositol phosphates was investigated using thyroids preloaded with [3H]inositol. Noradrenaline increased [3H]inositol accumulation into inositol phosphates in the mouse thyroid during a 30-min incubation whereas TSH (10 mU/ml) was without effect. The effect of noradrenaline was mimicked by phenylephrine, but not by clonidine or isoprenaline. Prazosin antagonized the effect of noradrenaline, while yohimbine had no effect. These results suggest that noradrenaline-induced production of inositol phosphates is mediated by alpha 1-adrenoceptors. The inhibition of release of thyroid hormones elicited by alpha 1-adrenergic agonists in the mouse thyroid is possibly mediated through the hydrolysis of membrane phosphoinositides followed by the generation of second messengers such as inositol phosphates and diacylglycerol.

Key concepts: Endocrinology, Internal medicine, Inositol, Thyroid, Inositol phosphate, Adrenergic receptor, Chemistry, Receptor

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