Hoffman W E, Phillips M I, Schmid P G
Am J Physiol. 1977 Apr;232(4):H426-33. doi: 10.1152/ajpheart.1977.232.4.H426.
The brain isorenin angiotensin system has been implicated in the development of spontaneous hypertension by several investigators. The experiments reported here were designed to test the responsiveness of unanesthetized spontaneous hypertensive (SH) rats to intracerebroventricular angiotensin II injections compared to Wistar-Kyoto (WK) normotensive controls. The results indicate that there is no difference between SH and WK animals in drinking responses or antidiuretic hormone release to central angiotensin II injections; however, an increased pressor responsiveness to intraventricular angiotensin II in SH as compared to WK was observed. The results of intravenous infusions of pressor substances in these experiments and reports by other investigators suggest that the increased blood pressure effects to central angiotensin are due to three possible factors: 1) increased vascular responsiveness of SH to vasoconstrictor substances in general, 2) increased vascular sensitivity of SH rats to sympathetic outflow, and 3) decreased baroreceptor reflexes to acute increases in blood pressure. We suggest that the brain isorenin-angiotensin system may be involved in spontaneous hypertension by increased production of angiotensin II or by activation of a potentiated sympathetic system, but not by a generalized increased sensitivity of brain receptors to central angiotensin.
几位研究者认为脑肾素血管紧张素系统与自发性高血压的发生有关。本文报道的实验旨在测试未麻醉的自发性高血压（SH）大鼠与Wistar-Kyoto（WK）正常血压对照大鼠相比，对脑室内注射血管紧张素II的反应性。结果表明，SH大鼠和WK大鼠在饮水反应或对中枢注射血管紧张素II的抗利尿激素释放方面没有差异；然而，与WK大鼠相比，观察到SH大鼠对脑室内血管紧张素II的升压反应性增加。这些实验中静脉输注升压物质的结果以及其他研究者的报告表明，对中枢血管紧张素的血压升高作用增加可能归因于三个可能的因素：1）一般而言，SH大鼠对血管收缩物质的血管反应性增加；2）SH大鼠对交感神经传出的血管敏感性增加；3）压力感受器对血压急性升高的反射减弱。我们认为，脑肾素血管紧张素系统可能通过血管紧张素II产生增加或通过增强的交感神经系统激活而参与自发性高血压，而不是通过脑受体对中枢血管紧张素的普遍敏感性增加。
