Site at which angiotensin II acts to stimulate ACTH secretion in vivo.
Site at which angiotensin II acts to stimulate ACTH secretion in vivo.
复制标题
血管紧张素 II 刺激体内 ACTH 分泌的位点。
DOI：
10.1159/000124824
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发表时间：
1987
影响因子：
4.1
通讯作者：
Ganong,WF
中科院分区：
文献类型：
--
作者：
Murakami,K;Ganong,WF
为了研究血管紧张素II （AII）增加促肾上腺皮质激素（ACTH）分泌的部位，在有意识的雄性大鼠中，研究了脑室内注射（IVT）或静脉注射（IV） AII拮抗剂saralasin对IVT或IV注射AII时ACTH反应的影响。AII不会穿过血脑屏障，但IVT和IV saralasin已知可以阻止循环AII与心室周围器官的结合。IV AII （0.2 - 200ng）诱导促肾上腺皮质激素（ACTH）分泌量呈剂量相关性增加，中隆起促肾上腺皮质激素释放激素（CRH）含量短暂升高。静脉注射salalasin（10µg）阻断ACTH对静脉注射AIL的反应，同样剂量的静脉注射salalasin对静脉注射AIL的ACTH反应没有产生类似的降低，而静脉注射1和10 ng AII则以剂量相关的方式增加血浆ACTH。静脉滴注色拉拉西素（12µg/kg/min）对静脉注射血管紧张素引起的血浆ACTH升高无抑制作用。另一方面，静脉输注该剂量的色拉色拉素可消除或降低ACTH对静脉注射大剂量AII的反应。这些数据支持循环AII通过作用于心室周围器官增加CRH分泌来刺激ACTH分泌的结论。他们还认为血脑屏障内的AII受体以及心室周围器官中的AII受体触发ACTH分泌增加。
To investigate the site at which angiotensin II (AII) acts to increase adrenocorticotrophic hormone (ACTH) secretion, the effects of intraventricular (IVT) or intravenous (IV) injection of the AII antagonist saralasin on the ACTH responses to IVT or IV injection of AII were examined in conscious male rats. AII does not cross the blood-brain barrier, but IVT as well as IV saralasin are known to prevent the binding of circulating AII to circumventricular organs. IV AII (0.2–200 ng) induced dose-related increases in ACTH secretion and a transient increase in the corticotrophin-releasing hormone (CRH) content of the median eminence. IVT injection of saralasin (10 µg) blocked the ACTH responses to IV AIL The same dose of saralasin given intravenously did not produce a comparable decrease in the ACTH response to IV AIL IVT injection of 1 and 10 ng AII increased plasma ACTH in a dose-related manner. The increase in plasma ACTH induced by IVT administration of angiotensin was not inhibited by IV infusion of saralasin (12 µg/kg/min). On the other hand IV infusion of this dose of saralasin abolished or reduced the ACTH response to IV injection of larger doses of AII. These data support the conclusion that circulating AII stimulates ACTH secretion by acting on the circumventricular organs to increase CRH secretion. They also suggest that AII receptors inside the blood-brain barrier as well as AII receptors in the circumventricular organs trigger increases in ACTH secretion.