氯沙坦和卡维地洛对Sprague Dawley大鼠体循环肾上腺素能激动剂和血管紧张素II血管加压反应的影响

M. H. Abdulla, M. A. Sattar, N. A. Abdullah, M. A. H. Khan, K. R. L. Anand Swarup, E. J. Johns
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引用次数: 5

摘要

1通过对正常大鼠血管紧张素II (Ang II)和肾上腺素能受体的累积阻断,探讨肾素-血管紧张素(RAS)与交感神经系统(SNS)的相互作用。2大鼠口服氯沙坦(10 mg/kg)、卡维地洛(5 mg/kg)或氯沙坦+卡维地洛(10 + 5 mg/kg),连续7 d。第8天,用戊巴比酮麻醉动物,准备进行全身血流动力学研究。测定静脉注射去甲肾上腺素(NA)、苯肾上腺素(PE)、甲氧苄胺(ME)和Angⅱ后平均动脉压升高或心率(HR)变化的剂量-反应关系。氯沙坦或氯沙坦与卡维地洛联用可减弱ME和angii的血管加压反应。除氯沙坦与卡维地洛联用外,所有治疗均显著抑制了激动剂对肺活量的影响。卡维地洛降低了NA、PE和Ang II的血管加压反应,降低了NA、ME和Ang II的HR反应。联合治疗对血管加压剂和HR反应的影响与氯沙坦相似,但对ME和Ang II的血管加压剂反应以及NA和Ang II的HR反应的影响比单独卡维地洛更大。由此得出结论,Ang II诱导的外周血管收缩部分是由肾上腺素能作用介导的,而肾上腺素能激动剂的血管加压反应依赖于完整的RAS。这些观察结果表明RAS和SNS在决定“正常”大鼠的全身血流动力学反应方面存在相互作用关系。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The effect of losartan and carvedilol on vasopressor responses to adrenergic agonists and angiotensin II in the systemic circulation of Sprague Dawley rats

1 Interaction between renin-angiotensin (RAS) and sympathetic nervous systems (SNS) was investigated by examining the effect of cumulative blockade of angiotensin II (Ang II) and adrenergic receptors in normal Sprague Dawley rats.

2 Rats were treated with losartan (10 mg/kg), carvedilol (5 mg/kg), or losartan plus carvedilol (10 + 5 mg/kg) orally for 7 days. On day 8, the animals were anaesthetized with pentobarbitone and prepared for systemic haemodynamic study. Dose–response relationships for the elevation of mean arterial pressure or change in heart rate (HR) in response to intravenous injections of noradrenaline (NA), phenylephrine (PE), methoxamine (ME) and Ang II were determined.

3 Losartan or the combination of losartan with carvedilol blunted vasopressor responses to ME and Ang II. Dose–response relationships for agonist action on HR were significantly inhibited by all treatments except for the combination of losartan and carvedilol on the decrease in HR induced by PE. Carvedilol decreased vasopressor responses to NA, PE and Ang II, and HR responses to NA, ME and Ang II. Combination treatment produced similar effects to losartan on the vasopressor and HR responses but had a greater effect on vasopressor responses to ME and Ang II, and on HR responses to NA and Ang II than carvedilol alone.

4 It is concluded that peripheral vasoconstriction induced by Ang II is partly mediated by adrenergic action and that the vasopressor responses to adrenergic agonists depend on an intact RAS. These observations suggest an interactive relationship between RAS and SNS in determining systemic haemodynamic responses in ‘normal’ rats.

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