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中枢血管紧张素II和血管紧张素III对压力反射调节的作用。

Effects of central angiotensin II and angiotensin III on baroreflex regulation.

作者信息

Appenrodt E, Brattström A

机构信息

Institute of Physiology, School of Medicine, Magdeburg, Germany.

出版信息

Neuropeptides. 1994 Mar;26(3):175-80. doi: 10.1016/0143-4179(94)90127-9.

Abstract

In the present study the cardiovascular effects of intracerebroventricularly (i.c.v.) applied angiotensin II (AN II) and angiotensin III (AN III) were analysed in conscious Wistar rats. The baroreceptor heart reflex (BHR) was elicited by intravenous bolus injection of both phenylephrine (1 microgram) and sodium nitroprusside (5 micrograms) before and after i.c.v. administration (1.5 and 15 min) of the peptides. Administration of 20 ng and 200 ng AN II produced a short increase in inter-beat interval (IBI) and a long-lasting increase in mean blood pressure (MBP), inclusive of a drinking response. Only after the high dose of 200 ng AN II we found a continuous impairment in the BHR for reflex bradycardia. Inversely, the small doses of both 100 pg AN II and 100 pg AN III were without effects on IBI and MBP; they induced an enhancement in BHR for the reflex bradycardia and after 100 pg AN II it was also found for the reflex tachycardia. Pretreatment with 20 nmol amastatin (AM), a specified aminopeptidase A inhibitor, followed by 100 pg An II suppressed the enhancement in BHR. AM alone was without effects in this respect. These findings suggest that: 1) the influence of central angiotensin on the BHR could be dose-dependent in the opposite way and 2) AN III seems to be the active form and involved in the central blood pressure regulatory mechanism.

摘要

在本研究中,分析了在清醒的Wistar大鼠中脑室内(i.c.v.)注射血管紧张素II(AN II)和血管紧张素III(AN III)对心血管系统的影响。在脑室内注射(1.5分钟和15分钟)肽类前后,通过静脉推注去氧肾上腺素(1微克)和硝普钠(5微克)引发压力感受器心脏反射(BHR)。注射20纳克和200纳克AN II会使心动周期(IBI)短暂增加,平均血压(MBP)持续升高,包括饮水反应。仅在注射高剂量200纳克AN II后,我们发现BHR对反射性心动过缓存在持续损害。相反,小剂量的100皮克AN II和100皮克AN III对IBI和MBP无影响;它们会增强BHR对反射性心动过缓的反应,并且在注射100皮克AN II后,对反射性心动过速也有增强作用。用20纳摩尔阿马astatin(AM)(一种特定的氨肽酶A抑制剂)预处理,然后注射100皮克AN II,可抑制BHR的增强。单独使用AM在这方面无影响。这些发现表明:1)中枢血管紧张素对BHR的影响可能呈相反的剂量依赖性;2)AN III似乎是活性形式,并参与中枢血压调节机制。

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