Wright J W, Morseth S L, Abhold R H, Harding J W
Am J Physiol. 1985 Nov;249(5 Pt 2):R514-21. doi: 10.1152/ajpregu.1985.249.5.R514.
The primary brain sites responsible for angiotensin-induced pressor action and dipsogenicity in the laboratory rat appear to be located in forebrain circumventricular organs (CVO). Because CVOs have a reduced blood-brain barrier, intracarotid infusion of angiotensin via a brachial arterial catheter results in direct stimulation of these sites. This investigation determined that brachial arterial infusion of angiotensin II (ANG II) into alert free-moving rats resulted in pressor and dipsogenic responses greater than those observed with equivalent doses of angiotensin III (ANG III). However, intracerebroventricular (ICV) injections of ANG II and ANG III yielded equivalent pressor and drinking responses. ICV pretreatment with the specific angiotensin receptor antagonist [Sar1, Ile8]-ANG II significantly reduced ANG II- and ANG III-induced pressor and drinking responses. This inhibition lasted approximately 20 min with recovery at 60-70 min. The results indicate that ICV-administered ANG III is a much more potent ligand than previously determined if the stickiness due to electrical charge of this compound is prevented by appropriate treatment of glassware. The receptor antagonist results encourage the possibility that ANG II and ANG III activate a common central receptor site.
在实验大鼠中，负责血管紧张素诱导的升压作用和致渴作用的主要脑区似乎位于前脑室周器官（CVO）。由于CVO的血脑屏障减弱，通过肱动脉导管进行颈内动脉血管紧张素灌注可直接刺激这些部位。本研究确定，向清醒自由活动的大鼠肱动脉灌注血管紧张素II（ANG II）所产生的升压和致渴反应大于同等剂量血管紧张素III（ANG III）所观察到的反应。然而，脑室内（ICV）注射ANG II和ANG III产生的升压和饮水反应相当。用特异性血管紧张素受体拮抗剂[Sar1，Ile8]-ANG II进行ICV预处理可显著降低ANG II和ANG III诱导的升压和饮水反应。这种抑制持续约20分钟，在60 - 70分钟时恢复。结果表明，如果通过对玻璃器皿进行适当处理来防止该化合物因电荷产生的黏性，那么ICV给药的ANG III是一种比先前确定的更有效的配体。受体拮抗剂的结果提示ANG II和ANG III激活共同的中枢受体位点的可能性。
