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Glucocorticoids down-regulate somatostatin receptors on pituitary cells in culture.

GH4C1 cells, a clonal strain of rat pituitary tumor cells which synthesize and secrete PRL and GH, have specific functional receptors for the two hypothalamic peptides TRH and somatostatin (SRIF). Chronic treatment of GH4C1 cells with cortisol has previously been shown to increase the number of TRH receptors per GH4C1 cell. The results reported here demonstrate that cortisol also causes a 20–40% decrease in the specific binding of [125I-Tyr1]SRIF. Treatment of GH4C1 cells with 5 × 10-6 M cortisol caused a time-dependent decrease in [125I-Tyr1]SRIF-specific binding. A maximal effect was achieved after 8 h of treatment, and the effect persisted for at least 48 h. Receptor affinity was the same in control and cortisol-pretreated cells (Kd = 7.8 × 10-10 M), but the number of SRIF-binding sites decreased from 21,900 to 15,20 receptors/cell. The half-maximal decrease in [125I-Tyr1]SRIF-specific binding occurred with 3 × 10-8 M cortisol. Pretreatment of cells with 5 × 10-7 M dexamethasone(1,4-pregnadien-9-fluoro...