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二硫苏糖醇对大鼠门静脉和兔主动脉中由1型血管紧张素受体介导的血管紧张素II诱导的收缩的抑制作用。

Inhibitory effect of dithiothreitol on angiotensin II-induced contractions mediated by AT1-receptors in rat portal vein and rabbit aorta.

作者信息

Zhang J S, van Meel J C, Pfaffendorf M, van Zwieten P A

机构信息

Department of Pharmacotherapy, Academic Medical Centre, University of Amsterdam, The Netherlands.

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1994 May;349(5):538-42. doi: 10.1007/BF00169144.

Abstract

The disulfide-reducing agent dithiothreitol (DTT) has been shown to reduce angiotensin II (Ang II) subtype 1 receptor (AT1) binding sites in various tissues. Its effect on Ang II-induced contractions was studied in the rat portal vein and rabbit aorta. In the isolated rat portal vein, DTT shifted the concentration-response curve for Ang II to the right (DTT 0.5-3 mmol/l) and depressed the maximal response (DTT 1-3 mmol/l). DTT 5 mmol/l almost abolished the effect of Ang II. In the isolated rabbit aorta, the inhibitory effect of DTT was more pronounced and its pattern of effect was different, since DTT 0.3 and 0.5 mmol/l caused a progressive flattening of the concentration-response curve of Ang II. DTT (1 mmol/l) fully suppressed the effect of Ang II. A biphasic curve consisting of a high sensitivity component and a component of low sensitivity for Ang II was observed after pretreatment with DTT 1 mmol/l in the rat portal vein but not in the rabbit aorta. In the presence of DTT 1 mmol/l, the AT1-receptor antagonist losartan antagonized the high sensitivity response to Ang II in a competitive manner with a pA2 value very similar to that obtained in the absence of DTT, suggesting that this response to Ang II is mediated by those AT1-receptors which were not inactivated by DTT. The biphasic curve may be explained by the occurrence of a single AT1-receptor subtype existing in two different states. Another possibility might be the involvement of two AT1-receptor subpopulations.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

二硫苏糖醇(DTT)这种二硫键还原剂已被证明可减少多种组织中的血管紧张素II(Ang II)1型受体(AT1)结合位点。研究了其对Ang II诱导的大鼠门静脉和兔主动脉收缩的影响。在离体大鼠门静脉中,DTT使Ang II的浓度 - 反应曲线右移(DTT 0.5 - 3 mmol/L)并降低最大反应(DTT 1 - 3 mmol/L)。5 mmol/L的DTT几乎消除了Ang II的作用。在离体兔主动脉中,DTT的抑制作用更明显且作用模式不同,因为0.3和0.5 mmol/L的DTT使Ang II的浓度 - 反应曲线逐渐变平。1 mmol/L的DTT完全抑制了Ang II的作用。在大鼠门静脉中用1 mmol/L的DTT预处理后观察到由高敏感性成分和低敏感性成分组成的双相曲线,但在兔主动脉中未观察到。在1 mmol/L的DTT存在下,AT1受体拮抗剂氯沙坦以竞争性方式拮抗对Ang II的高敏感性反应,其pA2值与在无DTT时获得的值非常相似,表明对Ang II的这种反应是由未被DTT灭活的那些AT1受体介导的。双相曲线可能由处于两种不同状态的单一AT1受体亚型的存在来解释。另一种可能性可能是涉及两个AT1受体亚群。(摘要截短于250字)

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