VASOACTIVE-INTESTINAL-PEPTIDE AND PEPTIDE WITH N-TERMINAL HISTIDINE AND C-TERMINAL ISOLEUCINE INCREASE PROLACTIN SECRETION IN CULTURED RAT PITUITARY-CELLS (GH4C1) VIA A CAMP-DEPENDENT MECHANISM WHICH INVOLVES TRANSIENT ELEVATION OF INTRACELLULAR CA-2+

VASOACTIVE-INTESTINAL-PEPTIDE AND PEPTIDE WITH N-TERMINAL HISTIDINE AND C-TERMINAL ISOLEUCINE INCREASE PROLACTIN SECRETION IN CULTURED RAT PITUITARY-CELLS (GH4C1) VIA A CAMP-DEPENDENT MECHANISM WHICH INVOLVES TRANSIENT ELEVATION OF INTRACELLULAR CA-2+
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DOI:
10.1016/0303-7207(87)90205-x
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发表时间:
1987-02-01
影响因子:
4.1
通讯作者:
HAUG, E
HAUG, E
中科院分区:
医学2区
文献类型:
--
作者:
BJORO, T;OSTBERG, BC;HAUG, E

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血管活性肠肽(VIP)和具有N-末端组氨酸和C-末端异亮氨酸(PHI)的肽(P)刺激GH4 C1细胞分泌催乳素(PRL)的效力相当,ED 50值为30-50 nM。在一个parafterm系统优化,以提供高的时间分辨率VIP和PHI增加PRL分泌延迟约60秒,随后激活的腺苷酸环化酶。甲状腺素(TRH)在4秒内增加催乳素(PRL)的分泌。VIP和PHI刺激的cAMP积累的剂量-反应曲线与PRL分泌的剂量-反应曲线重叠。在次最大浓度的VIP和PHI对cAMP的积累和PRL分泌的影响是加性的,而在浓度最大的影响是不加性的。VIP和PHI增加[Ca 2 +]i测量quin-2在不同的方式比TRH,不诱导的GH4 C1细胞的电生理膜特性的变化。我们的结论是,VIP和PHI刺激PRL分泌通过cAMP依赖性的过程,涉及增加[Ca 2 +]i。
Vasoactive intestinal peptide (VIP) and peptide (P) with N-terminal histidine and C-terminal isoleucine (PHI) stimulated prolactin (PRL) secretion from GH4C1 cells equipotent with ED50 values of 30-50 nM. In a parafusion system optimized to give high time resolution both VIP and PHI increased PRL secretion with a delay of about 60 s and subsequent to the activation of the adenylate cyclase. Thyroliberin (TRH) increased PRL secretion within 4 s. The dose-response curves for VIP- and PHI-stimulated cAMP accumulation were superimposable on those for PRL secretion. At submaximal concentrations the effects of VIP and PHI on both cAMP accumulation and PRL secretion were additive, whereas the effects were not additive at concentrations giving maximal effects. VIP and PHI increased [Ca2+]i measured by quin-2 in a different way than TRH, without inducing changes in the electrophysiological membrane properties of the GH4C1 cells. We conclude that both VIP and PHI stimulate PRL secretion via a cAMP-dependent process involving an increase in [Ca2+]i.