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体外灌流大鼠胃中内源性去甲肾上腺素的释放:突触前和突触后肾上腺素能受体的调节作用

Release of endogenous noradrenaline from the vascularly perfused rat stomach in vitro: modulation by pre- and postsynaptic adrenoceptors.

作者信息

Yokotani K, Okuma Y, Osumi Y

机构信息

Department of Pharmacology, Kochi Medical School, Japan.

出版信息

J Pharmacol Exp Ther. 1992 Feb;260(2):728-33.

PMID:1346643
Abstract

We developed an experimental in vitro model to detect a very small amount of endogenous noradrenaline (NA) released from the rat gastric sympathetic nerve terminals. The stomach was perfused via celiac artery with modified Krebs-Ringer solution containing 10 mM pargyline and 0.1% bovine serum albumin at a constant flow of 4 ml/min. The right greater splanchnic (SPL) nerve (preganglionic nerve of the gastric sympathetic nerve) was stimulated electrically with square-wave pulses of 2 msec duration and supramaximal intensity (5 mA) for 1 min. The rat stomach contained about 750 ng of NA and spontaneous overflow was about 0.05% of tissue content per 2 min. The NA overflow induced by SPL nerve stimulation at 5 Hz was abolished by tetrodotoxin (3 x 10(-7) M) and by Ca(++)-free medium containing 2 mM ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid. Hexamethonium (5 x 10(-4) M) significantly decreased the NA overflow induced by SPL nerve stimulation at 5 Hz. Yohimbine (10(-7) and 10(-6) M) and prazosin (10(-7) and 10(-6) M) dose-dependently enhanced the NA overflow induced by SPL nerve stimulation at 5 Hz. Clonidine (10(-7) and 10(-6) M) and methoxamine (10(-5) M) significantly decreased the NA overflow induced by SPL nerve stimulation at 1 Hz and this methoxamine-induced inhibition was abolished by 8-(p-sulfophenyl)-theophylline (5 x 10(-5) M).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

我们建立了一种体外实验模型,用于检测从大鼠胃交感神经末梢释放的极少量内源性去甲肾上腺素(NA)。通过腹腔动脉以4毫升/分钟的恒定流速用含有10毫摩尔优降宁和0.1%牛血清白蛋白的改良Krebs-Ringer溶液灌注胃。用持续时间为2毫秒、强度为超最大强度(5毫安)的方波脉冲电刺激右侧内脏大神经(胃交感神经的节前神经)1分钟。大鼠胃中含有约750纳克NA,每2分钟的自发溢出量约为组织含量的0.05%。5赫兹时内脏大神经刺激诱导的NA溢出被河豚毒素(3×10⁻⁷摩尔)和含有2毫摩尔乙二醇双(β-氨基乙醚)-N,N'-四乙酸的无钙培养基所消除。六甲铵(5×10⁻⁴摩尔)显著降低了5赫兹时内脏大神经刺激诱导的NA溢出。育亨宾(10⁻⁷和10⁻⁶摩尔)和哌唑嗪(10⁻⁷和10⁻⁶摩尔)剂量依赖性地增强了5赫兹时内脏大神经刺激诱导的NA溢出。可乐定(10⁻⁷和10⁻⁶摩尔)和甲氧明(10⁻⁵摩尔)显著降低了1赫兹时内脏大神经刺激诱导的NA溢出,并且这种甲氧明诱导的抑制作用被8-(对磺基苯基)茶碱(5×10⁻⁵摩尔)消除。(摘要截断于250字)

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