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内源性阿片肽在最后区升压途径中的作用。

The role of endogenous opiates in the area postrema pressor pathway.

作者信息

Szilagyi J E, Ferrario C M

出版信息

Clin Sci (Lond). 1980 Dec;59 Suppl 6:267s-269s. doi: 10.1042/cs059267s.

Abstract
  1. Intra-vertebral artery-administered angiotensin II acts at the area postrema to facilitate central sympathetic vasomotor activity. Recent evidence suggests a possible role of the opiate system in the mechanism of action of angiotensin II at the level of the brain stem. 2. In these experiments, we show that the morphine antagonist naloxone reduces significantly the magnitude of the pressor response to vertebral artery-infused angiotensin II. 3. Morphine, in contrast, doubled the peak of the vertebral response to identical doses of the peptide. Neither naloxone nor morphine affected the pressor responses to intravenously administered angiotensin II. 4. The data suggest that the endogenous opiate system in the medulla modulates the cardiovascular effects of angiotensin II at the level of the area postrema.
摘要
  1. 经椎动脉给予的血管紧张素II作用于最后区,以促进中枢交感缩血管活动。最近的证据表明,阿片系统在血管紧张素II于脑干水平的作用机制中可能发挥作用。2. 在这些实验中,我们表明吗啡拮抗剂纳洛酮可显著降低对经椎动脉注入的血管紧张素II的升压反应幅度。3. 相比之下,吗啡使对相同剂量该肽的椎动脉反应峰值增加了一倍。纳洛酮和吗啡均未影响对静脉注射血管紧张素II的升压反应。4. 数据表明,延髓中的内源性阿片系统在最后区水平调节血管紧张素II的心血管效应。

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