Biphasic release of thyrotropin in response to thyrotropin-releasing hormon (TRH) from rat anterior pituitary cells in vitro: Possible dependence on protein synthesis.

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Abstract
Mechanisms related to the biphasic release of TSH were studied using primary cultured cells of the rat anterior pituitary gland on micro-carrier beads in a superfusion system. Release of TSH in response to continuous exposure to TRH exhibited a biphasic pattern; the 1st phase was characterized by a rapid, transient and high rate release (phase I) and the 2nd phase by a chronic and low rate release (phase II). The shift of the release from phase I to phase II occurred by treatment with TRH at concentrations from submaximal to maximal. When the Ca2+ concentration in the medium was decreased, the phase I release was partially inhibited, while the phase II release was completely inhibited, suggesting a difference between the mechanisms in phase I and phase II relesae. The phase I release was not suppressed by cycloheximide. This protein synthesis-independent release of phase I seemed to be linked to the intracellular releasable pool of TSH. The phase II release was suppressed by the presence of a protein synthesis inhibitor. After the phase II release was suppressed by cycloheximide, the magnitude of phase I release in response to reexposure to TRH markedly decreased. The decreased phase I release in response to TRH was observed with the cells which were previously stimulated by high K+ instead of TRH, suggesting that the decrease in the response of phase I reflects the depletion of a releasable pool of TSH rather than homologous desensitization of thyrotrophs with TRH. Apparently, the phase I release of TSH depends on a portion of the previously prepared-releasable pool, while phase II release depends on previously prepared plus newly prepared pools of TSH. Replenishment of the releasable TSH pool was considered to involve protein synthesis.

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