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Exaggerated circadian variation in basal thyrotropin (TSH) and in the dopaminergic inhibition of TSH release in pathological hyperprolactinemia: evidence against a hypothalamic dopaminergic defect.
J Clin Endocrinol Metab. 1983 Nov; 57(5):975-80.JC

Abstract

In order to delineate more accurately the dopaminergic control of anterior pituitary function in normal subjects and in patients with pathological hyperprolactinemia, we investigated the nature of the circadian variation in the dopaminergic inhibition of TSH release in such subjects. Ten euthyroid women with hyperprolactinemia due to presumed PRL-secreting microadenomas (aged 18-60 yr) were compared with 11 normal, euthyroid women (aged 18-32 yr). Each received the dopamine receptor blocking drug domperidone (10 mg, iv) at 1100 and 2300 h (tests randomized and separated by at least 1 week). Blood was sampled 10, 20, 30, 45, and 60 min after drug administration. Normal women had a greater TSH response to domperidone and, hence, greater dopaminergic inhibition of TSH release at 2300 than at 1100 h (sum of TSH increments; mU/liter mean +/- SE, 8.5 +/- 1.3 vs. 4.8 +/- 0.5, P less than 0.01), whereas there was no difference in the dopaminergic inhibition of PRL release at each time of day. Hyperprolactinemic women also had a significantly greater TSH response to domperidone at 2300 than at 1100 h (42.0 +/- 10.2 vs. 19.1 +/- 2.8, P less than 0.001). The hyperprolactinemic women had a greater TSH response to domperidone than normal women at each time of day studied (1100 h, 19.1 +/- 2.8 vs. 4.8 +/- 0.5, P less than 0.001; 2300 h, 42.0 +/- 10.2 vs. 8.5 +/- 1.3, P less than 0.001). The incremental PRL responses to domperidone were significantly less in hyperprolactinemic than in normal women and did not differ at each time of day. In conclusion, the circadian change in the dopaminergic inhibition of TSH secretion is specific for TSH and not PRL. This indicates that the dopaminergic control of TSH and PRL secretion can be dissociated in normal subjects. Second, hyperprolactinemic women with presumed PRL-secreting microadenomas had qualitatively normal but quantitatively exaggerated circadian pattern of dopaminergic inhibition of TSH release. These data argue against a hypothalamic dopaminergic defect in hyperprolactinemia and support the view that the established dopaminergic defect in the inhibition of PRL release is related specifically to PRL control and may well be at the anterior pituitary level.

Authors

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Pub Type(s)

Clinical Trial
Journal Article
Randomized Controlled Trial

Language

eng

PubMed ID

6619271

Citation

Rodriguez-Arnao, M D., et al. "Exaggerated Circadian Variation in Basal Thyrotropin (TSH) and in the Dopaminergic Inhibition of TSH Release in Pathological Hyperprolactinemia: Evidence Against a Hypothalamic Dopaminergic Defect." The Journal of Clinical Endocrinology and Metabolism, vol. 57, no. 5, 1983, pp. 975-80.
Rodriguez-Arnao MD, Peters JR, Foord SM, et al. Exaggerated circadian variation in basal thyrotropin (TSH) and in the dopaminergic inhibition of TSH release in pathological hyperprolactinemia: evidence against a hypothalamic dopaminergic defect. J Clin Endocrinol Metab. 1983;57(5):975-80.
Rodriguez-Arnao, M. D., Peters, J. R., Foord, S. M., Dieguez, C., Edwards, C., Gomez-Pan, A., Hall, R., Newcombe, R. G., & Scanlon, M. F. (1983). Exaggerated circadian variation in basal thyrotropin (TSH) and in the dopaminergic inhibition of TSH release in pathological hyperprolactinemia: evidence against a hypothalamic dopaminergic defect. The Journal of Clinical Endocrinology and Metabolism, 57(5), 975-80.
Rodriguez-Arnao MD, et al. Exaggerated Circadian Variation in Basal Thyrotropin (TSH) and in the Dopaminergic Inhibition of TSH Release in Pathological Hyperprolactinemia: Evidence Against a Hypothalamic Dopaminergic Defect. J Clin Endocrinol Metab. 1983;57(5):975-80. PubMed PMID: 6619271.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Exaggerated circadian variation in basal thyrotropin (TSH) and in the dopaminergic inhibition of TSH release in pathological hyperprolactinemia: evidence against a hypothalamic dopaminergic defect. AU - Rodriguez-Arnao,M D, AU - Peters,J R, AU - Foord,S M, AU - Dieguez,C, AU - Edwards,C, AU - Gomez-Pan,A, AU - Hall,R, AU - Newcombe,R G, AU - Scanlon,M F, PY - 1983/11/1/pubmed PY - 1983/11/1/medline PY - 1983/11/1/entrez SP - 975 EP - 80 JF - The Journal of clinical endocrinology and metabolism JO - J Clin Endocrinol Metab VL - 57 IS - 5 N2 - In order to delineate more accurately the dopaminergic control of anterior pituitary function in normal subjects and in patients with pathological hyperprolactinemia, we investigated the nature of the circadian variation in the dopaminergic inhibition of TSH release in such subjects. Ten euthyroid women with hyperprolactinemia due to presumed PRL-secreting microadenomas (aged 18-60 yr) were compared with 11 normal, euthyroid women (aged 18-32 yr). Each received the dopamine receptor blocking drug domperidone (10 mg, iv) at 1100 and 2300 h (tests randomized and separated by at least 1 week). Blood was sampled 10, 20, 30, 45, and 60 min after drug administration. Normal women had a greater TSH response to domperidone and, hence, greater dopaminergic inhibition of TSH release at 2300 than at 1100 h (sum of TSH increments; mU/liter mean +/- SE, 8.5 +/- 1.3 vs. 4.8 +/- 0.5, P less than 0.01), whereas there was no difference in the dopaminergic inhibition of PRL release at each time of day. Hyperprolactinemic women also had a significantly greater TSH response to domperidone at 2300 than at 1100 h (42.0 +/- 10.2 vs. 19.1 +/- 2.8, P less than 0.001). The hyperprolactinemic women had a greater TSH response to domperidone than normal women at each time of day studied (1100 h, 19.1 +/- 2.8 vs. 4.8 +/- 0.5, P less than 0.001; 2300 h, 42.0 +/- 10.2 vs. 8.5 +/- 1.3, P less than 0.001). The incremental PRL responses to domperidone were significantly less in hyperprolactinemic than in normal women and did not differ at each time of day. In conclusion, the circadian change in the dopaminergic inhibition of TSH secretion is specific for TSH and not PRL. This indicates that the dopaminergic control of TSH and PRL secretion can be dissociated in normal subjects. Second, hyperprolactinemic women with presumed PRL-secreting microadenomas had qualitatively normal but quantitatively exaggerated circadian pattern of dopaminergic inhibition of TSH release. These data argue against a hypothalamic dopaminergic defect in hyperprolactinemia and support the view that the established dopaminergic defect in the inhibition of PRL release is related specifically to PRL control and may well be at the anterior pituitary level. SN - 0021-972X UR - https://www.unboundmedicine.com/medline/citation/6619271/Exaggerated_circadian_variation_in_basal_thyrotropin__TSH__and_in_the_dopaminergic_inhibition_of_TSH_release_in_pathological_hyperprolactinemia:_evidence_against_a_hypothalamic_dopaminergic_defect_ L2 - https://academic.oup.com/jcem/article-lookup/doi/10.1210/jcem-57-5-975 DB - PRIME DP - Unbound Medicine ER -