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心房利钠因子与西氯他宁对内皮素和去氧肾上腺素诱导的离体大鼠主动脉收缩的相互作用

[Interaction of atrial natriuretic factor and cicletanine in relation to contractions induced by endothelin and phenylephrine on the isolated rat aorta].

作者信息

Auguet M, Delaflotte S, Braquet P

机构信息

Institut Henri-Beaufour/IPSEN, Le Plessis-Robinson, France.

出版信息

Arch Mal Coeur Vaiss. 1989 Nov;82 Spec No 4:59-62.

PMID:2532880
Abstract

The interaction between cicletanine (CIC) and atrial natriuretic factor (ANF) on vessels was studied using the isolated rat aorta as model. Contractions induced by endothelin (ET1), a vasoconstrictor peptide from vascular endothelial cells, and by phenylephrine (PE), an alpha 1-adrenoceptor agonist, were recorded isometrically on aortic rings the endothelium of which had deliberately been damaged. Both agonists produced a concentration-dependent contraction (ET1:EC50 1.8 nM, Emax 2.2 g; PE:EC50 30 nM, Emax 2.4 g) which was antagonized by a 30 min pretreatment with either CIC (100 microM) or ANF (1 nM). However, PE was more sensitive than ET1 to the inhibitory action of CIC or ANF. Moreover, during inhibition by ANF spasmodic contractions were observed with PE but not with ET1; this was not observed when the antagonist was CIC. The inhibitory effect produced by the combination of CIC and ANF was additive with ET1 whereas a potentiation was observed with PE. Thus, on the isolated rat aorta model the contraction induced by PE was more sensitive to the action of ANF than that induced by ET1, which indicates that the two antagonists have a different mechanism of action. A direct action of CIC on the alpha-adrenoceptor might account for the potentiation observed between ANF and CIC against PE.

摘要

以离体大鼠主动脉为模型,研究了西氯他宁(CIC)与心钠素(ANF)在血管上的相互作用。使用故意损伤内皮的主动脉环,等长记录由血管内皮细胞产生的血管收缩肽内皮素(ET1)和α1 -肾上腺素能受体激动剂去氧肾上腺素(PE)诱导的收缩。两种激动剂均产生浓度依赖性收缩(ET1:EC50 1.8 nM,Emax 2.2 g;PE:EC50 30 nM,Emax 2.4 g),用CIC(100 μM)或ANF(1 nM)预处理30分钟可拮抗该收缩。然而,PE对CIC或ANF的抑制作用比ET1更敏感。此外,在ANF抑制期间,观察到PE会出现痉挛性收缩,而ET1则不会;当拮抗剂为CIC时未观察到此现象。CIC和ANF联合产生的抑制作用与ET1呈相加作用,而与PE则观察到增强作用。因此,在离体大鼠主动脉模型上,PE诱导的收缩比ET1诱导的收缩对ANF的作用更敏感,这表明两种拮抗剂具有不同的作用机制。CIC对α -肾上腺素能受体的直接作用可能解释了ANF和CIC对PE的增强作用。

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