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心房利钠肽对大鼠下丘脑 - 神经垂体复合体β-内啡肽释放的影响。

Effect of atrial natriuretic peptide on the release of beta-endorphin from rat hypothalamo-neurohypophysial complex.

作者信息

Ikeda Y, Tanaka I, Oki Y, Ikeda Y, Yoshimi T

机构信息

Second Department of Internal Medicine, Hamamatsu University School of Medicine, Japan.

出版信息

Endocrinol Jpn. 1989 Oct;36(5):647-53. doi: 10.1507/endocrj1954.36.647.

Abstract

The aim of this study was to determine whether atrial natriuretic peptide (ANP) alters beta-endorphin (beta-END) secretion from rat intermediate pituitary and whether this effect is a direct action on the intermediate pituitary or an indirect one mediated by hypothalamic factor(s). We studied the release of beta-END from rat neuro-intermediate lobes of the pituitary (NIL) and from the hypothalamo-neurohypophysial complex (HNC), which consists of the hypothalamus, pituitary stalk, intermediate and posterior lobes of the pituitary, by means of an in vitro perifusion system. NIL and HNC were prepared from male Wistar rats and individually perifused for 30 min with perifusion medium followed by 20 min perifusion with medium containing alpha-rat ANP and/or dopamine (DA). Samples of perifusion medium were collected every 5 min and subjected to RIA for beta-END. The basal release of beta-END from NIL was 180% of that from HNC (p less than 0.01), which provides further support for the presence of hypothalamic factors that inhibit beta-END release from the intermediate pituitary. The perifusion of HNC with ANP at 10(-7) and 10(-6) M increased the beta-END concentration by 25 and 50%, respectively (p less than 0.01). In contrast, ANP (10(-8) to 10(-6) M) had no effect on beta-END release from NIL. The inhibitory effect of DA (10(6) M) on beta-END release from NIL and HNC (51% and 50% of the basal release, respectively, p less than 0.01) was confirmed. However, this inhibitory effect was not reversed by ANP.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

本研究的目的是确定心房利钠肽(ANP)是否会改变大鼠垂体中间叶β-内啡肽(β-END)的分泌,以及这种作用是对垂体中间叶的直接作用还是由下丘脑因子介导的间接作用。我们通过体外灌流系统研究了大鼠垂体神经中间叶(NIL)和下丘脑-神经垂体复合体(HNC,由下丘脑、垂体柄、垂体中间叶和后叶组成)中β-END的释放。从雄性Wistar大鼠制备NIL和HNC,先用灌流培养基单独灌流30分钟,然后用含α-大鼠ANP和/或多巴胺(DA)的培养基灌流20分钟。每隔5分钟收集灌流培养基样品,并进行β-END的放射免疫分析(RIA)。NIL中β-END的基础释放量是HNC的180%(p<0.01),这进一步支持了存在抑制垂体中间叶β-END释放的下丘脑因子。用10^(-7)和10^(-6) M的ANP灌流HNC,β-END浓度分别增加25%和50%(p<0.01)。相比之下,ANP(10^(-8)至10^(-6) M)对NIL中β-END的释放没有影响。DA(10^(-6) M)对NIL和HNC中β-END释放的抑制作用(分别为基础释放量的51%和50%,p<0.01)得到证实。然而,ANP并不能逆转这种抑制作用。(摘要截断于250字)

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