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Hypothalamic Regulation of Pulsatile Thyrotopin Secretion^*

Department of Clinical Endocrinology, Medizinische Hochschule Hannover, Germany

Address all correspondence and requests for reprints to: G. Brabant,Department of Clinical Endocrinology, Medizinische Hochschule Hannover, Konstanty-Gutschowstr. 8, D-3000 Hannover 61, Germany.

To determine the mechanism underlying pulsatile TSH secretion, 24-h serum TSH levels were measured in three groups of five healthy volunteers by sampling blood every 10 min. The influence of an 8-h infusion of dopamine (200 mg), somatostatin (500 µg), or nifedipine (5 mg) on the pulsatile release of TSH was tested using a cross-over design. The amount of TSH released per pulse was significantly lowered by these drugs, resulting in significantly decreased mean basal TSH serum levels. However, pulses of TSH were still detectable at all times. The TSH response to TRH (200 µg) tested in separate experiments was significantly lowered after 3 h of nifedipine infusion compared to the saline control value. Nifedipine treatment did not alter basal, pulsatile, or TRH-stimulated PRL secretion. The persistence of TSH pulses under dopamine and somatostatin treatment and the blunted TSH response to nifedipine infusion support the hypothesis that pulsatile TSH secretion is under the control of hypothalamic TRH. The 24-h TSH secretion pattern achieved under stimulation with exogenous TRH in two patients with hypothalamic destruction through surgical removal of a craniopharyngioma provided further circumstantial evidence for this assumption. No TSH pulses and low basal TSH secretion were observed under basal conditions (1700–2400 h), whereas subsequent repetitive TRH challenge (25 µg/2 h to 50 µg/1 h) led to a pulsatile release of TSH with fusion of TSH pulses, resulting in a TSH secretion pattern strikingly similar to the circadian variation. These data suggest that pulsatile and circadian TSH secretions are predominantly controlled by TRH.

^* Parts of this work were presented in abstract form at the 17th Annual Meeting of the European Thyroid Association, Montpellier, France 1988, and at the International Congress of Endocrinology, Tokyo, Japan 1988. This work was supported by DFG Grant 915/1-1 and in part by Henning Berlin.

Received May 9, 1990.

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