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Differential Effects of Somatostatin (SRIH) and a SRIH Analog, SMS 201-995, on the Secretion of Growth Hormone and Thyroid-Stimulating Hormone in Man^*

Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Cincinnati College of Medicine Cincinnati, Ohio 45267

Address all correspondence and requests for reprints to: Timothy C. Williams, M.D., Division of Endocrinology and Metabolism, ML 547, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267.

We compared the ability of SRIH and SRIH analog, SMS 201-995 (SMS), to inhibit stimulated GH and TSH secretion in men who received 120-min iv infusions of saline, SRIH (5, 50, and 500 µg/h), and SMS (3, 30, and 300 ng/kgh) together with a bolus iv injection of GHRH (1 µg/kg) and TRH (500 µg). Integrated GH secretion during the 60 min after GHRH plus TRH injection was decreased compared to that after saline by (mean ± SE) 32 ± 14% (P = 0.059), 78 ± 5% (P < 0.001), and 88 ± 3% (P < 0.001) during the 5, 50, and 500 µg/h SRIH infusions, and by 13 ± 7% (P = NS), 50 ± 15% (P < 0.05), and 80 ± 6% (P < 0.001) during the 3, 30, and 300 ng/kgh SMS infusions. In contrast, integrated TSH secretion was unaltered during the 5 µg/h SRIH and 3 ng/kgh SMS infusions; it decreased by only 43 ± 5% (P < 0.001) and 66 ± 4% (P < 0.001) during the 50 and 500 ng/h SRIH infusions and by 33 ± 8% (P < 0.05) and 50 ± 3% (P < 0.001) during the 30 and 300 ng/kgh SMS infusions. Analysis of the dose-response curves indicated approximately 10- and 5-fold greater potencies of SRIH and SMS, respectively, in inhibiting GH as compared to TSH secretion. These results quantify the effect of SRIH as an inhibitor of GH secretion and suggest that if SRIH has a physiological role in the inhibition of TSH secretion in man, it is limited to conditions associated with marked suppression of GH.

^* This work was supported in part by USPHS Grants DK-30667 and RR-00068. Portions of this work were presented at the 1986 National Meeting of the American Federation for Clinical Research, Washington, D.C.

Received December 14, 1987.

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