Fink G D, Haywood J R, Bryan W J, Packwood W, Brody M J
Am J Physiol. 1980 Sep;239(3):R358-61. doi: 10.1152/ajpregu.1980.239.3.R358.
A previous study demonstrated that the threshold dose of intra-arterial angiotensin II required to induce a pressor response in the rat was significantly lower when the drug was administered into the carotid artery than when administered into the abdominal aorta. This result was interpreted to indicate that part of the increase in arterial pressure produced by low concentrations of blood-borne angiotensin in this species was the result of an effect on structures in the central nervous system selectively accessible via the carotid vascular bed. The purpose of the present study was to establish more precisely the site of the pressor action of angiotensin within the central nervous system. The central component of the pressor effect of angiotensin was quantified as the difference in pressor responses to intracarotid and intra-aortic infusions of angiotensin II (delta c-a). In conscious rats, delta c-a was attenuated by administration of the angiotensin antagonist, saralasin, into the third cerebral ventricle. In rats with chronic electrolytic lesions of the anteroventral third ventricle (AV3V), delta c-a was abolished. Periventricular structures surrounding the third ventricle appear to mediate the central component of the pressor action of blood-borne angiotensin in the rat.
先前的一项研究表明，将药物注入大鼠颈动脉时，诱导其产生升压反应所需的动脉内血管紧张素II的阈值剂量，显著低于将药物注入腹主动脉时的阈值剂量。该结果被解释为表明，在该物种中，低浓度血源性血管紧张素所产生的动脉血压升高，部分是由于对通过颈动脉血管床可选择性进入的中枢神经系统结构产生作用的结果。本研究的目的是更精确地确定血管紧张素在中枢神经系统内的升压作用位点。血管紧张素升压作用的中枢成分，被量化为颈动脉内和主动脉内输注血管紧张素II时升压反应的差异（δc-a）。在清醒大鼠中，向第三脑室注射血管紧张素拮抗剂沙拉新可减弱δc-a。在前腹侧第三脑室（AV3V）有慢性电解损伤的大鼠中，δc-a消失。围绕第三脑室的室周结构似乎介导了大鼠血源性血管紧张素升压作用的中枢成分。
