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Interrelationship between Thyroxine and Estradiol on the Secretion of Thyrotropin-Releasing Hormone and Dopamine into Hypophysial Portal Blood in Ovariectomized-Thyroidectomized Rats

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Effects of thyroxine (T<sub>4</sub>) on the secretion of thyrotropin-releasing hormone (TRH) and catecholamines into hypophysial portal blood and on the concentrations of arterial plasma thyroid-stimulating hormone (TSH) and prolactin (PRL) in ovariectomized and thyroidectomized (Ovx-Tx) rats were studied. Immediately after ovariectomy, rats were Tx or sham Tx. The Ovx-Tx rats were injected subcutaneously with estradiol benzoate (EB, 0.5 µg/kg b.w.) or sesame oil, and T<sub>4</sub> (20 µg/kg b.w.) or saline once daily for 2 weeks. The Ovx rats with intact thyroid gland were injected with saline and oil only. The hypophysial portal blood samples were collected and mixed with or without 2, 3-dimercaptopropanol before extraction by methanol or perchloric acid, respectively. The femoral arterial blood was also collected. The concentrations of TRH in methanol-extracted portal plasma and that of TSH and PRL in arterial plasma were measured by radioimmunoassay. The concentrations of catecholamines in perchloric acid-extracted portal plasma samples were measured by radioenzymatic assay. Thyroidectomy in Ovx rats resulted in an increase in portal plasma TRH and arterial plasma TSH. Despite the presence or absence of estradiol, T<sub>4</sub> replacement in Ovx-Tx rats decreased portal plasma TRH and arterial plasma TSH to euthyroid levels. Combination of the injection of T<sub>4 </sub>and EB in vivo caused significantly decreased levels of portal plasma dopamine and increased arterial plasma PRL compared with those in vehicle-injected Ovx-Tx animals. Concentrations of neither norepinephrine nor epinephrine in hypophysial portal plasma paralleled the altered concentrations of PRL or TSH in arterial plasma. These findings indicate that the negative feedback control of thyroid hormones on the secretion of pituitary TSH is due, at least in part, to inhibition of secretion of TRH into hypophysial portal blood, and that thyroxine potentiates the stimulatory effect of estradiol on the secretion of pituitary PRL by inhibition of secretion of dopamine into hypophysial portal blood.
Title: Interrelationship between Thyroxine and Estradiol on the Secretion of Thyrotropin-Releasing Hormone and Dopamine into Hypophysial Portal Blood in Ovariectomized-Thyroidectomized Rats
Description:
Effects of thyroxine (T<sub>4</sub>) on the secretion of thyrotropin-releasing hormone (TRH) and catecholamines into hypophysial portal blood and on the concentrations of arterial plasma thyroid-stimulating hormone (TSH) and prolactin (PRL) in ovariectomized and thyroidectomized (Ovx-Tx) rats were studied.
Immediately after ovariectomy, rats were Tx or sham Tx.
The Ovx-Tx rats were injected subcutaneously with estradiol benzoate (EB, 0.
5 µg/kg b.
w.
) or sesame oil, and T<sub>4</sub> (20 µg/kg b.
w.
) or saline once daily for 2 weeks.
The Ovx rats with intact thyroid gland were injected with saline and oil only.
The hypophysial portal blood samples were collected and mixed with or without 2, 3-dimercaptopropanol before extraction by methanol or perchloric acid, respectively.
The femoral arterial blood was also collected.
The concentrations of TRH in methanol-extracted portal plasma and that of TSH and PRL in arterial plasma were measured by radioimmunoassay.
The concentrations of catecholamines in perchloric acid-extracted portal plasma samples were measured by radioenzymatic assay.
Thyroidectomy in Ovx rats resulted in an increase in portal plasma TRH and arterial plasma TSH.
Despite the presence or absence of estradiol, T<sub>4</sub> replacement in Ovx-Tx rats decreased portal plasma TRH and arterial plasma TSH to euthyroid levels.
Combination of the injection of T<sub>4 </sub>and EB in vivo caused significantly decreased levels of portal plasma dopamine and increased arterial plasma PRL compared with those in vehicle-injected Ovx-Tx animals.
Concentrations of neither norepinephrine nor epinephrine in hypophysial portal plasma paralleled the altered concentrations of PRL or TSH in arterial plasma.
These findings indicate that the negative feedback control of thyroid hormones on the secretion of pituitary TSH is due, at least in part, to inhibition of secretion of TRH into hypophysial portal blood, and that thyroxine potentiates the stimulatory effect of estradiol on the secretion of pituitary PRL by inhibition of secretion of dopamine into hypophysial portal blood.

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