Suppr超能文献

内源性腺苷对大鼠输精管附睾段去甲肾上腺素释放的促进和抑制调节作用。

Facilitatory and inhibitory modulation by endogenous adenosine of noradrenaline release in the epididymal portion of rat vas deferens.

作者信息

Gonçalves J, Queiroz G

机构信息

Laboratório de Farmacologia, Faculdade de Farmácia da Universidade do Porto, Portugal.

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1993 Oct;348(4):367-71. doi: 10.1007/BF00171335.

Abstract

The present study aimed at determining the modulation by adenosine of the release of noradrenaline in the epididymal portion of the rat vas deferens. The tissues were treated with pargyline and perifused in the presence of desipramine and yohimbine. Up to four periods of electrical stimulation were applied (5 Hz, 9 min). The A1-adenosine receptor selective agonist R-N6-phenylisopropyladenosine (R-PIA; 100-900 nmol.l-1) reduced, whereas the A2A-receptor selective agonist 2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamidoadenosine (CGS 21680; 3-30 nmol.l-1) increased the electrically-evoked noradrenaline overflow in a concentration-dependent manner. The nonselective agonist 5'-N-ethylcarboxamidoadenosine (NECA; 30-300 nmol.l-1) reduced noradrenaline overflow, but the effect did not depend on the concentration. Adenosine deaminase at the concentration of 0.5 mu.ml-1 decreased but at that of 2.0 mu.ml-1 increased noradrenaline overflow. The inhibitors of adenosine uptake, S-(4-nitrobenzyl)-6-thioinosine (NBTI; 50 nmol.l-1) and dipyridamole (3 mumol.l-1), increased the electrically-evoked noradrenaline overflow. The A1-adenosine receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX; 20 nmol.l-1) caused an increase whereas the A2-adenosine receptor antagonist 3,7-dimethyl-1-(2-propynyl)xanthine (DMPX; 0.1 mumol.l-1) caused a decrease. NBTI (50 nmol.l-1), partially antagonized the effect of both DPCPX (20 nmol.l-1) and DMPX (0.1 mumol.l-1).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

本研究旨在确定腺苷对大鼠输精管附睾段去甲肾上腺素释放的调节作用。组织用帕吉林处理,并在存在地昔帕明和育亨宾的情况下进行灌流。施加高达四个电刺激周期(5Hz,9分钟)。A1-腺苷受体选择性激动剂R-N6-苯异丙基腺苷(R-PIA;100-900nmol·l-1)可降低,而A2A受体选择性激动剂2-p-(2-羧乙基)苯乙氨基-5'-N-乙基羧酰胺腺苷(CGS 21680;3-30nmol·l-1)以浓度依赖性方式增加电诱发的去甲肾上腺素溢出。非选择性激动剂5'-N-乙基羧酰胺腺苷(NECA;30-300nmol·l-1)可降低去甲肾上腺素溢出,但该作用不依赖于浓度。浓度为0.5μl/ml的腺苷脱氨酶可降低,但浓度为2.0μl/ml时可增加去甲肾上腺素溢出。腺苷摄取抑制剂S-(4-硝基苄基)-6-硫代肌苷(NBTI;50nmol·l-1)和双嘧达莫(3μmol·l-1)可增加电诱发的去甲肾上腺素溢出。A1-腺苷受体拮抗剂1,3-二丙基-8-环戊基黄嘌呤(DPCPX;20nmol·l-1)可导致增加,而A2-腺苷受体拮抗剂3,7-二甲基-1-(2-丙炔基)黄嘌呤(DMPX;0.1μmol·l-1)可导致减少。NBTI(50nmol·l-1)部分拮抗DPCPX(20nmol·l-1)和DMPX(0.1μmol·l-1)的作用。(摘要截短于250字)

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验