Inhibition of Thyrotropin Secretion by Physiological Levels of Corticosterone*
Richard W. Pamenter, George A. Hedge
Abstract
Richard W. Pamenter, George A. Hedge
Abstract
We have studied the effects of physiological amounts of the native glucocorticoid of the rat on basal and TRH-induced TSH secretion. Adrenalectomized rats received jugular and ip catheters 3 days before each experiment; the former was used for blood sampling and TRH administration, and the latter was used for constant corticosterone infusion in the absence of anesthesia or stress. Various levels of corticosterone within the range seen in intact rats (up to about 60 μg/dl) were maintained by varying the infusion rate, and plasma levels of corticosterone were documented in all cases by fluorometric assay. At different times after the onset of corticosterone infusion, pre-TRH and post-TRH (250 ng/100g BW) plasma samples were collected for RIA of TSH. No significant changes in basal TSH levels were observed. However, corticosterone in the lower half of its physiological range significantly inhibited the pituitary response to submaximal TRH stimulation both 10 and 30 min after the TRH. To verify that this is a direct pituitary effect, small amounts of corticosterone (50 ng) and TRH (1 ng) were sequentially infused stereotaxically directly into the anterior pituitaries of anesthetized rats. Such local infusions did not alter systemic corticosterone levels, but they did significantly inhibit the TSH response to local TRH. These findings indicate that, under stress-free conditions, physiological levels of the native glucocorticoid in the rat help regulate pituitary sensitivity to TRH. (Endocrinology106: 162, 1980)
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We have studied the effects of physiological amounts of the native glucocorticoid of the rat on basal and TRH-induced TSH secretion. Adrenalectomized rats received jugular and ip catheters 3 days before each experiment; the former was used for blood sampling and TRH administration, and the latter was used for constant corticosterone infusion in the absence of anesthesia or stress. Various levels of corticosterone within the range seen in intact rats (up to about 60 μg/dl) were maintained by varying the infusion rate, and plasma levels of corticosterone were documented in all cases by fluorometric assay. At different times after the onset of corticosterone infusion, pre-TRH and post-TRH (250 ng/100g BW) plasma samples were collected for RIA of TSH. No significant changes in basal TSH levels were observed. However, corticosterone in the lower half of its physiological range significantly inhibited the pituitary response to submaximal TRH stimulation both 10 and 30 min after the TRH. To verify that this is a direct pituitary effect, small amounts of corticosterone (50 ng) and TRH (1 ng) were sequentially infused stereotaxically directly into the anterior pituitaries of anesthetized rats. Such local infusions did not alter systemic corticosterone levels, but they did significantly inhibit the TSH response to local TRH. These findings indicate that, under stress-free conditions, physiological levels of the native glucocorticoid in the rat help regulate pituitary sensitivity to TRH. (Endocrinology106: 162, 1980)
Key concepts: Endocrinology, Internal medicine, Corticosterone, Secretion, Thyrotropin-releasing hormone, Medicine, Chemistry, Biology