Central administration of angiotensin II receptor antagonists and arterial pressure regulation: a note of caution.
Central administration of angiotensin II receptor antagonists and arterial pressure regulation: a note of caution.
复制标题
血管紧张素 II 受体拮抗剂的中枢给药和动脉压调节：注意事项。
DOI：
10.1016/0024-3205(92)90139-g
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发表时间：
1992
期刊：
影响因子：
6.1
通讯作者：
Eskridge-Sloop,SL
中科院分区：
文献类型：
--
作者：
Gruber,KA;Callahan,MF;Eskridge-Sloop,SL
在脑室内给予血管紧张素II（AII）拮抗剂后，动脉压对各种升压药的增加或某些高血压模型中动脉压的降低减弱，已被解释为这些情况下中枢AII系统参与的初步证据。加压素或卡巴胆碱（一种胆碱能激动剂）的中枢给药产生升压作用，据报道，这是由于交感神经系统活动的增加。我们现在报告，大鼠中枢给予AII拮抗剂[（Sar-1，Ile-8）AII或（Sar-1，Ala-8）AII]可阻止大部分（> 70%）心室内加压素或卡巴胆碱的升压作用。这些结果可以从两个方面来解释。首先，所有这些升压剂都使用中枢血管紧张素能机制来增加交感神经系统活动。另一种假设是，中枢给药的AII拮抗剂非特异性抑制交感神经系统功能。
The blunting of arterial pressure increases to a variety of pressor agents or the lowering of arterial pressure in some models of hypertension following intracerebroventricular administration of an angiotensin II (AII) antagonist, has been interpreted as prima facie evidence for the involvement of the central AII system in these situations. Central administration of vasopressin or carbachol (a cholinergic agonist) produces pressor effects which have been reported to be due to an increase in the activity of the sympathetic nervous system. We now report that central administration of AII antagonists [either (Sar-1, Ile-8) AII or (Sar-1, Ala-8) AII] in rats prevents the majority (> 70%) of the pressor effects of intraventricular vasopressin or carbachol. These results can be interpreted in two ways. The first is that all of these pressor agents use a central angiotensinergic mechanism (s) to increase sympathetic nervous system activity. An alternative hypothesis is that centrally administered AII antagonists non-specifically inhibit sympathetic nervous system function.