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外周血管紧张素II对穹窿下器和垂体神经叶的选择性代谢刺激作用。

Selective metabolic stimulation of the subfornical organ and pituitary neural lobe by peripheral angiotensin II.

作者信息

Gross P M, Kadekaro M, Andrews D W, Sokoloff L, Saavedra J M

出版信息

Peptides. 1985;6 Suppl 1:145-52. doi: 10.1016/0196-9781(85)90024-5.

Abstract

The subfornical organ is a major receptor area for one of the principal stimuli of thirst, the octapeptide, angiotensin II. In conscious water-sated rats, we examined the effects of intravenous infusion of angiotensin II on the rate of glucose utilization in the subfornical organ and in structures anatomically and functionally connected with it. Angiotensin II produced pressor and drinking responses and increased glucose utilization selectively in the subfornical organ and pituitary neural lobe and in no other brain structure. Treatment with the angiotensin II antagonist, sar1-leu8-angiotensin II, before intravenous administration of angiotensin II prevented metabolic stimulation of the subfornical organ and neural lobe. Captopril, an inhibitor of angiotensin-converting enzyme, was administered to homozygous Brattleboro rats, which normally have elevated rates of glucose utilization in the subfornical organ. Captopril reduced subfornical organ glucose metabolism to a level similar to that found in control animals. These results demonstrate that peripheral angiotensin II stimulates glucose metabolism in the subfornical organ under conditions in which it provokes drinking and pressor responses. The findings suggest that circulating angiotensin II is responsible for the high rate of glucose utilization observed in the subfornical organ of Brattleboro rats homozygous for diabetes insipidus.

摘要

穹窿下器官是主要的口渴刺激物之一——八肽血管紧张素II的主要受体区域。在清醒且水合状态良好的大鼠中,我们研究了静脉注射血管紧张素II对穹窿下器官以及与其在解剖学和功能上相连的结构中葡萄糖利用率的影响。血管紧张素II引起了升压和饮水反应,并选择性地增加了穹窿下器官、垂体神经叶中的葡萄糖利用率,而在其他脑结构中则没有。在静脉注射血管紧张素II之前,用血管紧张素II拮抗剂sar1-leu8-血管紧张素II进行处理,可防止穹窿下器官和神经叶的代谢受到刺激。给纯合布拉特洛维大鼠(其穹窿下器官中葡萄糖利用率通常较高)施用血管紧张素转换酶抑制剂卡托普利。卡托普利将穹窿下器官的葡萄糖代谢降低到与对照动物相似的水平。这些结果表明,在引发饮水和升压反应的条件下,外周血管紧张素II会刺激穹窿下器官中的葡萄糖代谢。这些发现表明,循环中的血管紧张素II是导致纯合尿崩症的布拉特洛维大鼠穹窿下器官中观察到的高葡萄糖利用率的原因。

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