In vivo and in vitro Effects of Cholecystokinin Octapeptide on the Release of β-Endorphin-Like Immunoreactivity

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Abstract
The effect of cholecystokinin octapeptide (CCK-8) on the release of β-endorphin-like immunoreactivity (β-EpLI) in rats was studied in vivo and in vitro. Intravenous injection of 5 μg/100 g body weight of CCK-8 resulted in significant increase in the plasma β-EpLI level after 10 and 20 min. CCK-8 at concentrations of 10–10–10–6M also caused dose-dependent stimulation of β-EpLI release from dispersed cells of rat anterior pituitary. However, CCK-4 and desulfated CCK-8 had no effect. On gel chromatography, the β-EpLI released by incubation of the cells with 10^8 MCCK-8 separated into two components, eluted in the same positions as human β-lipotropin and human β-endorphin, respectively. CCK-8 did not stimulate β-EpLI release in Ca++-free medium. A 23187 at concentrations of 10–6-10–3M caused dose-dependent stimulation of β-EpLI release from the cells. Addition of 2 × 10–3M CoCL, 10–3M verapamil or 10–7M dexamethasone to the incubation medium inhibited CCK-8-induced β-EpLI release from the cells. Dibutyryl cyclic GMP (3 × 10–3M) inhibited CCK-8-induced β-EpLI release from the cells. Ouabain (10–5M) also stimulated β-EpLI release but its effect was not additive with that of CCK-8. These results indicate that CCK-8 acts directly and specifically on anterior pituitary cells to stimulate β-EpLI release and that calcium ion is involved in the mechanism of this effect.