Effects of Somatostatin on the Secretion of Thyrotropin and Prolactin

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Abstract
Somatostatin, a tetradecapeptide isolated from ovine hypothalamic extracts on the basis of its ability to inhibit the spontaneous secretion of growth hormone (GH) by pituitary cell cultures, has been found to inhibit the stimulated secretion of thyrotropin (TSH) mediated by TRF(pGlu-His- Pro-NH2), 10 × [K†], or theophylline in vitro, while having no effect on the secretion of luteinizing hormone (LH) due to LRF. The spontaneous release of PRL in vitro is also inhibited by somatostatin but to a lesser extent than is the spontaneous secretion of GH. In vivo, the TRF-triggered secretion of TSH but not of PRL is suppressed by somatostatin in the estrogen-progesteronepretreated male rat. The injection of TRF leads to a greater rise in both plasma TSH and PRL in estrogen-progesterone-pretreated male rats than in untreated male rats. Somatostatin acts rapidly but reversibly to inhibit the secretion of TSH due to TRF in a dose-dependent manner. Thyroid hormones and somatostatin exhibit summation in their inhibition of TSH secretion in vivo and in vitro. These data indicate the potential for somatostatin, along with thyroid hormones and TRF, to play a physiological role in the regulation of TSH secretion. (Endocrinology95: 968, 1974)

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