Stimulatory and Inhibitory Action of Estradiol on TSH Secretion1

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Abstract
Subcutaneous administration of low doses of estradiol benzoate (EB: 0.004, 0.016, 0.064, 0.256 txg daily, 9–11 days) to rats ovariectomized for 28–30 days resulted in stimulation or inhibition of pituitary-thyroid function. The relatively low dose of 0.064 /xg elevated pituitary and plasma TSH levels and induced thyroid hyperplasia. A higher dose level (.256 μg) inhibited TSH secretion by the pituitary and caused involution of the thyroid gland. The biphasic action of estradiol of TSH secretion was not attributable to alterations in the thyroxine (T4) binding capacity of the blood proteins. Resin uptake of radiothyroxine from plasma was significantly decreased in rats treated with propylthiouracil (PTU) or in animals subjected to thyroidectomy, ovariectomy and hypothalamic lesioning. The administration of EB to hypothyroid rats failed to influence appreciably T4 resin uptake from plasma. In contrast, a critical dose level of EB (.02 μg daily, 7–8 days) stimulated TSH secretion in thyroidectomized, ovariectomized rats bearing median eminence lesions, whereas a 4-fold increase in dose (0.8 μg) reduced TSH concentration of plasma and pituitary to below control levels. It is concluded that the biphasic effect of estradiol on TSH secretion does not require the presence either of hypothalamic TRF or of circulating thyroid hormone but rather reflects a direct action of the steroid on the pituitary thyrotrophs. (Endocrinology88: 687, 1971)

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