Sim M K, Radhakrishnan R
Department of Pharmacology, Faculty of Medicine, National University of Singapore.
Eur J Pharmacol. 1994 May 12;257(1-2):R1-3. doi: 10.1016/0014-2999(94)90714-5.
Intracerebroventricularly administered des-Asp-angiotensin I, when prevented from degradation by prior administration of captopril, attenuated dose-dependently the central pressor actions of angiotensin II and angiotensin III in the spontaneously hypertensive (SHR) and Wistar Kyoto (WKY) rats. This finding is the first demonstration of an intrinsic action of des-Asp-angiotensin I and, together with earlier finding of its increased production in the hypothalamus of the spontaneously hypertensive rat, may support the suggestion that the nonapeptide is a functional angiotensin that regulates the pressor action of angiotensin II and angiotensin III in the brain.
脑室内注射去天冬氨酸血管紧张素I时,若预先给予卡托普利以防止其降解,则可剂量依赖性地减弱血管紧张素II和血管紧张素III对自发性高血压大鼠(SHR)和Wistar Kyoto大鼠(WKY)的中枢升压作用。这一发现首次证明了去天冬氨酸血管紧张素I的内在作用,并且与之前关于其在自发性高血压大鼠下丘脑产生增加的发现一起,可能支持以下观点:该九肽是一种功能性血管紧张素,可调节大脑中血管紧张素II和血管紧张素III的升压作用。