Le Mevel J C, Pamantung T F, Mabin D, Vaudry H
Laboratoire de Neurophysiologie, UFR de Médecine, Université de Bretagne Occidentale, Brest, France.
Brain Res. 1994 Aug 22;654(2):216-22. doi: 10.1016/0006-8993(94)90482-0.
The central effect of angiotensin II on cardiovascular activity has been investigated in conscious trout bearing an intracerebroventricular (i.c.v.) cannula and an intra-arterial catheter. I.c.v. injection of the angiotensin II agonist [Asn1,Val5]AII (6.2-50 pmol) induced a dose-dependent increase in heart rate and arterial blood pressure. Central administration of the angiotensin II antagonist DuP 753 (5 nmol) 30 min before i.c.v. injection of [Asn1,Val5]AII totally prevented the tachycardia and reduced the hypertension induced by the angiotensin II agonist. Intra-arterial injection of arginine-vasotocin (12.5 pmol) caused a bradycardia associated with a marked increase in arterial blood pressure. I.c.v. injection of [Asn1,Val5]AII totally blocked the bradycardia induced by arginine-vasotocin and this effect was prevented by central administration of DuP 753. In contrast, [Asn1,Val5]AII did not affect the increase in blood pressure induced by arginine vasotocin. Suppression of the vagal tone by atropine treatment totally blocked the central effect of [Asn1,Val5]AII. These results show that angiotensin II acts directly on the trout brain to increase blood pressure and heart rate. The effect of angiotensin II is mediated through a receptor related to the mammalian AT1 receptor type.
在有意识的、带有脑室内（i.c.v.）插管和动脉内导管的虹鳟鱼中，研究了血管紧张素II对心血管活动的中枢作用。脑室内注射血管紧张素II激动剂[Asn1,Val5]AII（6.2 - 50皮摩尔）可引起心率和动脉血压剂量依赖性升高。在脑室内注射[Asn1,Val5]AII前30分钟，中枢给予血管紧张素II拮抗剂DuP 753（5纳摩尔）可完全预防心动过速，并减轻血管紧张素II激动剂诱导的高血压。动脉内注射精氨酸 - 加压催产素（12.5皮摩尔）引起心动过缓，并伴有动脉血压显著升高。脑室内注射[Asn1,Val5]AII可完全阻断精氨酸 - 加压催产素诱导的心动过缓，且这种作用可被中枢给予DuP 753所预防。相反，[Asn1,Val5]AII不影响精氨酸 - 加压催产素诱导的血压升高。阿托品处理抑制迷走神经张力可完全阻断[Asn1,Val5]AII的中枢作用。这些结果表明，血管紧张素II直接作用于虹鳟鱼脑，以升高血压和心率。血管紧张素II的作用是通过与哺乳动物AT1型受体相关的受体介导的。
