Binding of angiotensin and atrial natriuretic peptide in brain of hypertensive rats
Binding of angiotensin and atrial natriuretic peptide in brain of hypertensive rats
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DOI：
10.1038/320758a0
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发表时间：
1986-04
期刊：
影响因子：
64.8
通讯作者：
J. Saavedra;F. Corrêa;L. Plunkett;A. Israel;M. Kurihara;K. Shigematsu
中科院分区：
文献类型：
--
作者：
J. Saavedra;F. Corrêa;L. Plunkett;A. Israel;M. Kurihara;K. Shigematsu
在哺乳动物心房中产生的心房利钠肽被释放到全身循环中，并可能作为外周血管紧张素系统的拮抗剂积极参与血压控制和流体稳态1 -4。心钠素的某些心血管作用可能是中枢介导的，因为心钠素（8-33）（ANF）的结合位点已定位于穹窿下器官5。这种脑室周围结构缺乏血脑屏障，因此可以进入循环肽。它含有大量的血管紧张素II（AII）结合位点，并被认为是循环AII调节血压和液体代谢的主要中心作用位点6，7。在此，我们通过定量放射自显影研究了自发性（遗传性）高血压大鼠（SHR）及其血压正常对照Wistar京都（WKY）大鼠8脑中大鼠心房利钠肽（6-33）（rANP）和AII的结合位点5，9-11。这两种肽的结合位点高度定位于穹隆下器官中。与年龄匹配的正常血压对照组相比，年轻（4周龄）和成年（14周龄）SHR穹窿下器官的rANP结合位点的数量减少。相反，AII结合位点的数量在年轻和成年SHR中均高于WKY大鼠。我们的研究结果表明，rANP和AII在遗传性高血压中的核心作用;它们可能在参与血压控制和液体调节的脑区中作为相互拮抗剂。
Atrial natriuretic peptides, produced in the mammalian cardiac atrium, are released into the general circulation and may be actively involved in the control of blood pressure and in fluid homeostasis as antagonists of the peripheral angiotensin system1–4. Certain cardiovascular effects of atrial natriuretic peptides may be centrally mediated, as binding sites for atrial natriuretic factor (8–33) (ANF) have been localized to the subfornical organ5. This circumventricular structure lacks a blood–brain barrier and is therefore accessible to circulating peptides. It contains large numbers of angiotensin II (AII) binding sites, and has been suggested as the main central site of action for circulating AII in the regulation of blood pressure and fluid metabolism6,7. Here we have studied binding sites for rat atrial natriuretic peptide(6–33) (rANP) and AII in the brains of spontaneously (genetic) hypertensive rats (SHR) and their normotensive controls, Wistar Kyoto (WKY) rats8, by quantitative autoradiography5,9–11. Binding sites for both peptides were highly localized in the subfornical organ. The number of rANP binding sites was decreased in the subfornical organ of both young (4 weeks old) and adult (14 weeks old) SHR compared with age-matched normotensive controls. Conversely, the number of AII binding sites was higher in both young and adult SHR compared with WKY rats. Our results suggest a central role for rANP and AII in genetic hypertension; they may act as mutual antagonists in brain areas involved in control of blood pressure and fluid regulation.