Prysor-Jones R A, Silverlight J J, Jenkins J S, Stevens A N, Rodrigues J L, Griffiths J R
FEBS Lett. 1984 Nov 5;177(1):71-5. doi: 10.1016/0014-5793(84)80983-7.
Intravenous thyrotrophin releasing hormone (TRH) caused a 6.5-fold increase in plasma prolactin (PRL) in rats carrying implanted pituitary tumours. Vasoactive intestinal polypeptide (VIP) had no effect, but TRH given after VIP raised TRH stimulated secretion 13-fold above basal. 31P NMR spectroscopy showed that VIP caused a decrease in high energy metabolites (depleted phosphocreatine, elevated inorganic phosphate and lowered intracellular pH). TRH alone caused a similar but smaller effect; given after VIP, it caused no detectable depletion. We suggest that the changes in high energy metabolite concentrations reflect increased cellular energy consumption consistent with a priming process (stage 1) in PRL secretion, followed by hormone release (stage 2). VIP induces stage 1 whereas RTH induced both stages.
静脉注射促甲状腺激素释放激素（TRH）可使植入垂体肿瘤的大鼠血浆催乳素（PRL）增加6.5倍。血管活性肠肽（VIP）无此作用，但在VIP之后给予TRH，可使TRH刺激的分泌比基础水平提高13倍。31P核磁共振波谱显示，VIP导致高能代谢物减少（磷酸肌酸耗尽、无机磷酸盐升高和细胞内pH降低）。单独给予TRH会产生类似但较小的作用；在VIP之后给予TRH，则不会导致可检测到的消耗。我们认为，高能代谢物浓度的变化反映了细胞能量消耗增加，这与PRL分泌的引发过程（第1阶段）一致，随后是激素释放（第2阶段）。VIP诱导第1阶段，而TRH诱导两个阶段。
