Angiotensin II acting on brain AT1 receptors induces adrenaline secretion and pressor responses in the rat.
Angiotensin II acting on brain AT1 receptors induces adrenaline secretion and pressor responses in the rat.
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DOI：
10.1038/srep07248
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发表时间：
2014-11-28
影响因子：
4.6
通讯作者：
Saito M
中科院分区：
文献类型：
--
作者：
Nakamura K;Shimizu T;Yanagita T;Nemoto T;Taniuchi K;Shimizu S;Dimitriadis F;Yawata T;Higashi Y;Ueba T;Saito M
血管紧张素II（AngII）在心血管功能的调节中起重要作用。AngII的外周和中枢作用都参与了这种调节，但后者作为脑内神经递质/神经调质的作用机制仍不清楚。在这里，我们表明（1）脑室（i. c. v.）在麻醉的雄性大鼠中给予血管紧张素II可升高源自肾上腺髓质的血浆肾上腺素，但不升高缬沙坦的去甲肾上腺素。（AT 1受体阻滞剂）敏感的脑机制，（2）外周AT 1受体不参与AngII诱导的血浆肾上腺素升高，尽管AngII诱导牛肾上腺髓质细胞分泌去甲肾上腺素和肾上腺素，（3）血管生成素II静脉注射可升高血压，但不升高心率，其机制与缬沙坦敏感有关。根据这些结果，i. c. v.给予AngII作用于脑AT 1受体，从而诱导肾上腺素分泌和升压反应。我们认为，中枢血管紧张素能系统可以激活中枢肾上腺髓质流出和调节血压。
Angiotensin II (AngII) plays important roles in the regulation of cardiovascular function. Both peripheral and central actions of AngII are involved in this regulation, but mechanisms of the latter actions as a neurotransmitter/neuromodulator within the brain are still unclear. Here we show that (1) intracerebroventricularly (i.c.v.) administered AngII in urethane-anesthetized male rats elevates plasma adrenaline derived from the adrenal medulla but not noradrenaline with valsartan- (AT1 receptor blocker) sensitive brain mechanisms, (2) peripheral AT1 receptors are not involved in the AngII-induced elevation of plasma adrenaline, although AngII induces both noradrenaline and adrenaline secretion from bovine adrenal medulla cells, and (3) i.c.v. administered AngII elevates blood pressure but not heart rate with the valsartan-sensitive mechanisms. From these results, i.c.v. administered AngII acts on brain AT1 receptors, thereby inducing the secretion of adrenaline and pressor responses. We propose that the central angiotensinergic system can activate central adrenomedullary outflow and modulate blood pressure.