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探讨ＳＨＲ及ＷＫＹ大鼠延髓腹外侧头端区（ｒｏｓｔｒａｌｖｅｎｔｒｏｌａｔｅｒａｌｍ ｅｄｕｌｌａ， ＲＶＬＭ）内微量注射血管紧张素Ⅱ（Ａｎｇ Ⅱ）和血管紧张素Ⅱ受体阻滞剂［Ｓａｒ１，Ｔｈｒ８］Ａｎｇ Ⅱ对心血管活动的影响。在ＳＨＲ及ＷＫＹ 大鼠，ＲＶＬＭ 微量注射人工脑脊液，不引起明显的心血管效应。ＲＶＬＭ 内微量注射递增剂量的Ａｎｇ Ⅱ（ｐｍ ｏｌ：０１，１０，１０，１００），引起血压升高，心率增加。两组实验动物血压、心率的变化无统计学差别。Ａｎｇ Ⅱ的效应可被预先注射［Ｓａｒ１，Ｔｈｒ８］Ａｎｇ Ⅱ所阻断。相反，ＲＶＬＭ 微量注射剂量递增的［Ｓａｒ１，Ｔｈｒ８］Ａｎｇ Ⅱ（ｐｍ ｏｌ：０１，１０，１０，１００），引起血压下降，心率减慢。在ＳＨＲ大鼠，血压下降的幅度明显大于ＷＫＹ大鼠，而心率的变化在两组动物中无显著差别。实验结果提示大鼠ＲＶＬＭ 内Ａｎｇ Ⅱ具有升高血压和增加心率的作用。Ａｎｇ Ⅱ的作用与Ａｎｇ Ⅱ受体介导有关。ＳＨＲ大鼠ＲＶＬＭ 内神经元对内源性Ａｎｇ Ⅱ的敏感性增高。ＳＨＲ大鼠高血压的形成与ＲＶＬＭ 内Ａｎｇ Ⅱ的升压作用增强有关。
To investigate the effects of angiotensin Ⅱ (Ang Ⅱ) and angiotensin Ⅱ receptor blocker (Ang1, Thr8) Ang Ⅱ on cardiovascular activity in rostral ventrolateral m edulla (RVLM) of SHR and WKY rats Impact. In SHR and WKY rats, microinjection of RVLM into artificial cerebrospinal fluid did not cause significant cardiovascular effects. Increasing dose of Ang Ⅱ (pmol: 0,1,1,0,0,10,100) in micro-injection of RVLM caused the increase of blood pressure and heart rate. There was no significant difference in blood pressure and heart rate between two groups of experimental animals. The effect of Ang Ⅱ can be blocked by pre-injection of [Sar1, Thr8] Ang Ⅱ. In contrast, RVLM microinjection of [Sar1, Thr8] AngII (pmol: 0.1, 1.0, 10, 100) caused a decrease in blood pressure and a decrease in heart rate. In SHR rats, blood pressure decreased significantly more than WKY rats, and heart rate changes in the two groups of animals no significant difference. Experimental results suggest that Ang Ⅱ in rat RVLM can increase blood pressure and increase heart rate. The role of Ang Ⅱ is mediated by Ang Ⅱ receptor. SHR rats RVLM neurons to endogenous Ang Ⅱ increased sensitivity. The formation of hypertension in SHR rats is related to the enhancement of the action of Ang Ⅱ in RVLM.