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Studies on the Response of Growth Hormone (GH) Secretion to GH-Releasing Hormone, Thyrotropin- Releasing Hormone, Gonadotropin-Releasing Hormone, and Somatostatin in Acromegaly^*

Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College 10 Ichigaya- Kawada-cho, Shinjuku-ku, Tokyo162
The Third Department of Internal Medicine, Nippon Medical School 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113, Japan
The Laboratories for Neuroendocrinobgy, The Salk Institute for Biological Studies La Jolla, California 92037

Address requests for reprints to: Tamotsu Shibasaki, M.D., Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women’s Medical College, 10 Ichigaya-Kawada-cho, Shinjuku-ku, Tokyo 162 Japan.

The plasma GH response to GH-releasirig hormone (GHRH), TRH, or GnRH administration was examined in 25 acromegalic patients. Plasma GH levels increased in 21 patients after GHRH, in 19 after TRH, and in 4 after G_nRH. The four GHRH nonresponders had had acromegaly longer than had the GHRH responders. No specific combination of GH responsiveness to these 3 releasing hormones was found among the patients. Infusion of 1 mg GHRH for 150 min gradually increased plasma GH levels, with some fluctuations, from the beginning to the end of infusion in normal subjects and in 7 patients who were GHRH responders, buta bolus injection of 100 g GHRH at the end of the infusion did not further elevate plasma GH levels. These results suggest that desensitization to GHRH occurred in the normal subjects and acromegalic patients. However, in 5 acromegalic patients who responded tobothGHRH and TRH, a bolus injection of 500 g TRH given at the end of the 150-min infusion of 1 mg GHRH evoked a further plasma GH rise. In 5 normal subjects and 2 patients who were responders to GHRH but not TRH, a bolus injection of 500 g TRH did not cause plasma GH elevation at the end of 150-min infusion of 1 mg GHRH. These results imply that TRH and GnRH stimulate GH secretion from the adenoma cells in vivo through receptors different from those for GHRH. In vitro studies using cultured pituitaryadenoma cells from 2 patients revealed that the responses of GH secretion to GHRH were similar to those in vivo. These data, therefore, suggest that the responsiveness of GH secretion to stimuli is determined by the specificity of the receptors on adenoma cells. The action of somatostatin-28 was more potent than that of somatostatin-14 in the suppression of GH secretion from adenoma cells.

^* This work was supported by a grant from the Japanese Ministry of Education, Science, and Culture; a research grant from the Intractable Diseases Division, Japanese Ministry of Health and Welfare; and NIH Grants HD-09690 and AM-18811.

Received May 1, 1985.

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