Suppr超能文献

去天冬氨酸血管紧张素I对正常和高血压大鼠主动脉环的作用。

Actions of des-Asp angiotensin I on the aortic rings of the normo- and hypertensive rats.

作者信息

Lim B C, Sim M K

机构信息

Department of Pharmacology, Faculty of Medicine National University of Singapore.

出版信息

Clin Exp Hypertens. 1998 Jan;20(1):105-17. doi: 10.3109/10641969809053210.

Abstract

The actions of des-Asp angiotensin I, a nine aminoacid peptide, on the contractility of the aortic rings of the normotensive Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) were studied. In the presence of captopril which prevented its degradation to angiotensin III by angiotensin converting enzyme, des-Asp-angiotensin I exerted direct concentration-dependent contractile action on the aortic rings. The contractile action was concentration-dependently attenuated by the AT1 receptor antagonist, losartan, but was not affected by the AT2 receptor antagonist, PD123319; indicating that angiotensin AT1 receptors mediate the direct contractile action. The response to des-Asp-angiotensin I was qualitatively different from that to angiotensin III i.e. lower potency and a likely higher efficacy suggesting that the two angiotensins act on different subtypes of angiotensin receptor. The response of the aortic rings to angiotensin III and des-Asp-angiotensin I in the SHR was significantly lower than the corresponding responses in WKY. Des-Asp-angiotensin I attenuated in a concentration-dependent and U-shape manner the response of the aortic ring to angiotensin III in the SHR but not in the WKY. Significant attenuation occurred in the pico to nano molar range of des-Asp-angiotensin I which is within the physiological concentration of the nonapeptide. Although these findings are the first demonstration of a direct and modulatory action of des-Asp-angiotensin I on the blood vessels of the SHR and raise the possibility of its involvement in blood pressure control, its exact role remains to be further studied.

摘要

研究了九肽去天冬氨酸血管紧张素I对正常血压的Wistar Kyoto大鼠(WKY)和自发性高血压大鼠(SHR)主动脉环收缩性的作用。在卡托普利存在的情况下,卡托普利可阻止其被血管紧张素转换酶降解为血管紧张素III,去天冬氨酸血管紧张素I对主动脉环产生直接的浓度依赖性收缩作用。AT1受体拮抗剂氯沙坦可浓度依赖性地减弱这种收缩作用,但AT2受体拮抗剂PD123319对其无影响;这表明血管紧张素AT1受体介导了这种直接的收缩作用。去天冬氨酸血管紧张素I的反应与血管紧张素III的反应在性质上不同,即效力较低且可能效力较高,这表明这两种血管紧张素作用于不同亚型的血管紧张素受体。SHR主动脉环对血管紧张素III和去天冬氨酸血管紧张素I的反应明显低于WKY中的相应反应。去天冬氨酸血管紧张素I以浓度依赖性和U形方式减弱SHR主动脉环对血管紧张素III的反应,但对WKY无此作用。在去天冬氨酸血管紧张素I的皮摩尔到纳摩尔范围内出现了显著减弱,这在该九肽的生理浓度范围内。尽管这些发现首次证明了去天冬氨酸血管紧张素I对SHR血管的直接调节作用,并增加了其参与血压控制的可能性,但其确切作用仍有待进一步研究。

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