Abstract
Out of 21 patients with active acromegaly, 12 increased plasma GH concentration after TRH injection (200 μg iv). No correlation was found between basal plasma GH levels, plasma GH response to hypoglycemia, arginine, oral glucose load and plasma GH response to TRH. The plasma GH peak often preceded that of TSH. One patient TSH unresponsive to TRH and 2 patients poorly responsive to TRH showed a rise in plasma GH. In 1 patient who increased both TSH and GH after TRH, the plasma TSH response was abolished by triiodothyronine administration, while that of plasma GH remained unchanged. Since it has been demonstrated that a releasing hormone acts activating the adenylcyclase system after binding to specific cellular receptors, it is suggested that in some functioning pituitary tumors the activity of TRH in promoting GH release may be attributed to an alteration of the cellular membrane. Another speculative possibility is that TRH acts at a hypothalamic rather than at a pituitary locus.
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