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多种阿片肽对大鼠垂体离体释放抗利尿激素和催产素的不同作用。

Differential effects of various opioid peptides on vasopressin and oxytocin release from the rat pituitary in vitro.

作者信息

Maysinger D, Vermes I, Tilders F, Seizinger B R, Gramsch C, Höllt V, Herz A

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1984 Dec;328(2):191-5. doi: 10.1007/BF00512071.

Abstract

Dynorphin (1-17), and to a lesser extent, beta-endorphin and [Leu]enkephalin (10(-6) M each) decreased the spontaneous release of vasopressin (VP) from the rat neurointermediate pituitary in vitro, whereas the oxytocin (OT) release remained unchanged. Naloxone, however, did not significantly alter the spontaneous VP and OT release. Dynorphin (1-17) (10(-7) M) increased the electrically evoked release of VP and OT, while 10(-6) M had a significant, somewhat less pronounced stimulatory effect only on VP, but not on OT release. The opiate inactive fragment [des-Tyr1]dynorphin (1-17) did not change the evoked VP and OT release, indicating that the dynorphin effect was mediated by opiate receptors. beta-Endorphin (10(-6) M and 10(-7) M) did not alter the evoked VP and OT secretion. 10(-6) M [Leu]enkephalin induced a stimulation of the evoked OT, but not VP release; 10(-7) M [Leu]enkephalin had no effect, neither on VP nor on OT release. The opiate antagonist naloxone (10(-5) M) induced an increase in the evoked VP and, even more pronounced, OT release. In a concentration of 10(-6) M, however, naloxone only increased the evoked OT release. When naloxone and dynorphin (1-17) were concomitantly applied, their stimulatory effects on the evoked VP and OT release were additive. Similarly to the effects of naloxone, addition of a monoclonal antibody which binds to the common N-terminal sequence of all endogenous opioid peptides, resulted in a marked increase in the evoked secretion of VP and, to an even more pronounced degree, of OT.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

强啡肽(1-17),以及程度稍轻的β-内啡肽和亮氨酸脑啡肽(各10⁻⁶ M)可降低大鼠神经垂体中间叶体外培养时血管加压素(VP)的自发释放,而催产素(OT)的释放保持不变。然而,纳洛酮并未显著改变VP和OT的自发释放。强啡肽(1-17)(10⁻⁷ M)可增加电刺激诱发的VP和OT释放,而10⁻⁶ M仅对VP有显著的、但不太明显的刺激作用,对OT释放无作用。阿片类无活性片段[去酪氨酸¹]强啡肽(1-17)不改变诱发的VP和OT释放,表明强啡肽的作用是由阿片受体介导的。β-内啡肽(10⁻⁶ M和10⁻⁷ M)不改变诱发的VP和OT分泌。10⁻⁶ M亮氨酸脑啡肽可刺激诱发的OT释放,但不刺激VP释放;10⁻⁷ M亮氨酸脑啡肽对VP和OT释放均无作用。阿片类拮抗剂纳洛酮(10⁻⁵ M)可增加诱发的VP释放,对OT释放的增加作用更明显。然而,在10⁻⁶ M浓度下,纳洛酮仅增加诱发的OT释放。当纳洛酮和强啡肽(1-17)同时应用时,它们对诱发的VP和OT释放的刺激作用是相加的。与纳洛酮的作用类似,添加一种与所有内源性阿片肽共同N端序列结合的单克隆抗体,可导致诱发的VP分泌显著增加,对OT分泌的增加作用更明显。(摘要截短至250字)

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