首页> 外文期刊>Life sciences >KAPPA OPIATE AGONIST RU 51599 INHIBITS VASOPRESSIN GENE EXPRESSION AND OSMOTICALLY-INDUCED VASOPRESSIN SECRETION IN VITRO
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KAPPA OPIATE AGONIST RU 51599 INHIBITS VASOPRESSIN GENE EXPRESSION AND OSMOTICALLY-INDUCED VASOPRESSIN SECRETION IN VITRO

机译:KAPPA阿片样物质激动剂RU 51599抑制血管加压素基因的表达和渗透诱导的血管加压素的体外分泌

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Kappa (kappa) opioid agonists induce a water diuresis acid inhibit vasopressin (AVP) secretion. Hypothalamic and neurohypophysial sites have both been implicated in the response. The present study was designed to ascertain if kappa-agonist inhibition of osmotically-stimulated AVP secretion is associated with parallel changes in AVP gene expression. Experiments were performed using the selective kappa-agonist RU 51599 (RU) in compartmentalized hypothalamo-neurohypophysial explants. When added to either the hypothalamus or the neural lobe, RU dose dependently inhibited osmotically-induced AVP secretion that was reversed by the highly selective kappa-antagonist nor-binaltorphimine (nor-BNI) only at the hypothalamic, not the neurohypophysial level. AVP mRNA content paralleled the changes in AVP secretory rate induced by hypothalamic kappa-agonism. AVP mRNA levels were unaltered when RU was applied to the neural lobe. Neurohypophysial AVP content did not change. These data indicate that hypothalamic kappa-agonism inhibits osmotically induced AVP secretion and that a non-kappa(1) opiate receptor mediates posterior pituitary opioid inhibition of AVP release. Neural or receptor inputs to the hypothalamus or magnocellular cell body may downwardly modulate AVP mRNA content by altering AVP gene transcription and/or message stability. Inhibition of AVP release directly at the neurohypophysis can be uncoupled from the cellular mechanisms that generate changes in AVP mRNA content. [References: 34]
机译:κ(阿片)阿片样物质激动剂诱导水利尿酸抑制血管加压素(AVP)分泌。下丘脑和神经下垂部位均与反应有关。本研究旨在确定渗透激动性AVP分泌的Kappa激动剂抑制是否与AVP基因表达的平行变化有关。使用选择性κ激动剂RU 51599(RU)在分隔的下丘脑-神经垂体外植体中进行实验。当添加到下丘脑或神经叶中时,RU剂量依赖性地抑制了渗透性诱导的AVP分泌,而高选择性的kappa拮抗剂nor-binaltorphimine(nor-BNI)只能在下丘脑而非神经下体水平上逆转渗透诱导的AVP分泌。 AVP mRNA含量与下丘脑κ-激动作用诱导的AVP分泌速率的变化平行。当RU应用于神经叶时,AVP mRNA水平未改变。神经垂体AVP含量未改变。这些数据表明下丘脑κ激动作用抑制渗透诱导的AVP分泌,并且非kappa(1)鸦片受体介导垂体后叶阿片样物质抑制AVP释放。下丘脑或大细胞细胞体的神经或受体输入可通过改变AVP基因转录和/或消息稳定性来向下调节AVP mRNA含量。直接在神经垂体处抑制AVP释放可以与产生AVP mRNA含量变化的细胞机制脱钩。 [参考:34]

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