Unger T, Rascher W, Schuster C, Pavlovitch R, Schömig A, Dietz R, Ganten D
Eur J Pharmacol. 1981 Apr 24;71(1):33-42. doi: 10.1016/0014-2999(81)90384-8.
The role of the sympathetic nervous system and of arginine vasopressin (AVP) in the mediation of the central cardiovascular effects of angiotensin II (ANG II) and substance P (SP) was investigated. ANG II and SP caused dose-dependent blood pressure increases when injected into the lateral brain ventricle (i.c.v.) of conscious rats; ANG II was tenfold more potent than SP. Peripheral blockade of alpha-adrenoceptors with prazosin or blockade of the vasopressor action of AVP by the AVP antagonist d(CH2)5VDAVP both partially inhibited the pressor responses to central ANG II. Combined treatment with the two blockers produced almost complete inhibition of the central ANG I responses. Substance P injected i.c.v. produced increases in noradrenaline and adrenaline but not AVP in the plasma. Peripheral alpha-receptor blockade by prazosin reversed the central pressor effects of SP to depressor responses. The AVP antagonist did not alter the cardiovascular responses to SP. It is concluded that in conscious animals, stimulation of the sympathetic nervous system and release of AVP contribute to the central pressor action of ANG II to a similar extent and independently of each other. In contrast, the central pressor responses to SP appear to be exclusively mediated by the sympathetic nervous system without participation of AVP.
研究了交感神经系统和精氨酸加压素（AVP）在介导血管紧张素II（ANG II）和P物质（SP）的中枢心血管效应中的作用。将ANG II和SP注入清醒大鼠的侧脑室（脑室内注射）时，会引起剂量依赖性的血压升高；ANG II的效力比SP强十倍。用哌唑嗪对外周α-肾上腺素能受体进行阻断，或用AVP拮抗剂d(CH2)5VDAVP阻断AVP的升压作用，均能部分抑制对中枢ANG II的升压反应。两种阻滞剂联合治疗几乎完全抑制了中枢ANG I反应。脑室内注射SP可使血浆中去甲肾上腺素和肾上腺素增加，但AVP不增加。哌唑嗪对外周α受体的阻断使SP的中枢升压作用逆转，变为降压反应。AVP拮抗剂并未改变对SP的心血管反应。得出的结论是，在清醒动物中，交感神经系统的刺激和AVP的释放对ANG II的中枢升压作用有相似程度的贡献，且彼此独立。相比之下，对SP的中枢升压反应似乎完全由交感神经系统介导，而无AVP的参与。
