Suppr超能文献

去窦弓神经大鼠肾上腺、垂体和脑内的血管紧张素II受体

Angiotensin II receptors in adrenal gland, pituitary gland and brain of sino-aortic denervated rats.

作者信息

Saavedra J M, Alexander N

出版信息

J Hypertens Suppl. 1986 Dec;4(5):S154-7.

PMID:3471898
Abstract

Angiotensin II (ANG II) binding sites were quantified in individual adrenal and pituitary glands and brain nuclei of sino-aortic denervated (neurogenically hypertensive) and sham-operated rats by incubation of 16-microns tissue sections with 125I-[Sar1] Ang II, autoradiography, computerized microdensitometry and comparison with 125I-standards. In the anterior pituitary, the number of ANG II binding sites (Bmax) was increased in sino-aortic denervated rats, 764 +/- 39 versus 2025 +/- 340 fmol/mg protein in sham-operated versus sino-aortic denervated. In the adrenal medulla the Bmax was decreased in sino-aortic denervated rats, 3313 +/- 71 versus 2736 +/- 181 fmol/mg protein in sham-operated versus sino-aortic denervated. There were no significant changes in adrenal zona glomerulosa ANG II binding capacity. In the nucleus of the solitary tract the Bmax was decreased, from 1422 +/- 22 fmol/mg protein in sham-operated to 370 +/- 52 fmol/mg protein in sino-aortic denervated rats. These results indicate that changes in ANG II binding occur in peripheral tissues and brain of neurogenic hypertensive rats. Our findings suggest that both peripheral and central ANG II may be associated with the pathophysiology of neurogenic hypertension.

摘要

通过将16微米厚的组织切片与125I-[Sar1]血管紧张素II孵育、放射自显影、计算机微密度测定法并与125I标准品进行比较,对去窦主动脉神经(神经源性高血压)大鼠和假手术大鼠的单个肾上腺、垂体以及脑核中的血管紧张素II(ANG II)结合位点进行了定量分析。在垂体前叶,去窦主动脉神经大鼠的ANG II结合位点数量(Bmax)增加,假手术组为2025±340飞摩尔/毫克蛋白,去窦主动脉神经组为764±39飞摩尔/毫克蛋白。在肾上腺髓质,去窦主动脉神经大鼠的Bmax降低,假手术组为3313±71飞摩尔/毫克蛋白,去窦主动脉神经组为2736±181飞摩尔/毫克蛋白。肾上腺球状带的ANG II结合能力没有显著变化。在孤束核中,Bmax降低,从假手术大鼠的1422±22飞摩尔/毫克蛋白降至去窦主动脉神经大鼠的370±52飞摩尔/毫克蛋白。这些结果表明,神经源性高血压大鼠的外周组织和脑中ANG II结合发生了变化。我们的研究结果表明,外周和中枢的ANG II都可能与神经源性高血压的病理生理学有关。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验