The renin-angiotensin system (RAS) is involved in cardiovascular and hydroelectrolytic control, being associated with the development of hypertension. The restraint stress (RS) model is an aversive situation, which promotes a sustained increase in blood pressure and heart rate, and stimulation of the hypothalamic–pituitary–adrenal axis. Stress leads to an increase of angiotensin-II contents both in the circulation and the central nervous system (CNS), as well as an increased expression of AT-1 receptors in CNS structures related to stress. Stressful stimuli are associated with the modulation of autonomic nervous system, as well as baroreflex; changes in this adjustment mechanism are related to cardiovascular diseases. We hypothesized that RAS is involved in the modulation of autonomic, neuroendocrine, and functional RS-caused alterations. The intravenous (i.v) pretreatment of rats with lisinopril, an angiotensin-converting-enzyme inhibitor, reduced the RS-evoked pressor response. The doses of 0.1 and 0.3 mg/kg also reduced the RS-evoked tachycardia, while in the dose of 1 mg/kg of lisinopril potentiated the tachycardic one. Additionally, i.v. pretreatment with losartan, a selective AT-1 receptor antagonist, reduced the pressor and the tachycardic responses caused by RS. Pretreatment with lisinopril 0.3 mg/kg increased the power of the low frequency (LF) band of the systolic BP spectrum after the treatment without affecting this parameter during RS. The pretreatment with losartan 1 mg/kg increased the power of the high frequency (HF) band and reduced the LF (n.u.) and the LF/HF ratio of the pulse interval spectrum in the first hour of RS. Concerning baroreflex sensitiveness (SBR), pretreatments with losartan or lisinopril did not affect the gain of the baroreflex sequences. However, the pretreatment with losartan reduced the baroreflex effectiveness index of the total sequences in the third hour of the RS. These results indicate that Ang-II, via the AT-1 receptor, plays a facilitating influence on the cardiovascular response caused by RS; facilitates sympathetic activation and reduces parasympathetic activity related to RS; facilitates the baroreflex activation during RS and favors corticosterone release under this stress model. The impairment of Ang-II synthesis, as well as the blockade of AT-1 receptors, may constitute an important pharmacological strategy to treat cardiovascular consequences caused by stress.

肾素-血管紧张素系统 (RAS) 参与心血管和水电解控制，与高血压的发展有关。约束压力 (RS) 模型是一种令人厌恶的情况，它会促进血压和心率的持续增加，并刺激下丘脑-垂体-肾上腺轴。压力导致循环和中枢神经系统 (CNS) 中血管紧张素 II 含量的增加，以及与压力相关的 CNS 结构中 AT-1 受体的表达增加。压力刺激与自主神经系统的调节以及压力反射有关；这种调节机制的变化与心血管疾病有关。我们假设 RAS 参与调节自主神经、神经内分泌和功能性 RS 引起的改变。用血管紧张素转换酶抑制剂赖诺普利对大鼠进行静脉内 (iv) 预处理，降低了 RS 诱发的升压反应。0.1 和 0.3 mg/kg 的剂量也降低了 RS 诱发的心动过速，而 1 mg/kg 的赖诺普利剂量增强了心动过速。此外，用选择性 AT-1 受体拮抗剂氯沙坦 iv 预处理可减少 RS 引起的升压和心动过速反应。赖诺普利 0.3 mg/kg 预处理增加了治疗后收缩压频谱的低频 (LF) 频带的功率，而在 RS 期间不影响该参数。氯沙坦1 mg/kg预处理​​增加了高频（HF）波段的功率，降低了RS第一小时脉冲间隔谱的LF（nu）和LF/HF比。关于压力反射敏感性（SBR），氯沙坦或赖诺普利预处理不影响压力反射序列的增益。然而，氯沙坦预处理降低了RS第三小时总序列的压力反射有效性指数。这些结果表明，Ang-II 通过 AT-1 受体对 RS 引起的心血管反应起到促进作用；促进交感神经激活并减少与 RS 相关的副交感神经活动；促进 RS 期间的压力反射激活，并有利于在这种压力模型下释放皮质酮。Ang-II 合成的损害以及 AT-1 受体的阻断可能构成治疗由压力引起的心血管后果的重要药理学策略。氯沙坦预处理降低了RS第三小时总序列的压力反射有效性指数。这些结果表明，Ang-II 通过 AT-1 受体对 RS 引起的心血管反应起到促进作用；促进交感神经激活并减少与 RS 相关的副交感神经活动；促进 RS 期间的压力反射激活，并有利于在这种压力模型下释放皮质酮。Ang-II 合成的损害以及 AT-1 受体的阻断可能构成治疗由压力引起的心血管后果的重要药理学策略。氯沙坦预处理降低了RS第三小时总序列的压力反射有效性指数。这些结果表明，Ang-II 通过 AT-1 受体对 RS 引起的心血管反应起到促进作用；促进交感神经激活并减少与 RS 相关的副交感神经活动；促进 RS 期间的压力反射激活，并有利于在这种压力模型下释放皮质酮。Ang-II 合成的损害以及 AT-1 受体的阻断可能构成治疗由压力引起的心血管后果的重要药理学策略。对 RS 引起的心血管反应有促进作用；促进交感神经激活并减少与 RS 相关的副交感神经活动；促进 RS 期间的压力反射激活，并有利于在这种压力模型下释放皮质酮。Ang-II 合成的损害以及 AT-1 受体的阻断可能构成治疗由压力引起的心血管后果的重要药理学策略。对 RS 引起的心血管反应有促进作用；促进交感神经激活并减少与 RS 相关的副交感神经活动；促进 RS 期间的压力反射激活，并有利于在这种压力模型下释放皮质酮。Ang-II 合成的损害以及 AT-1 受体的阻断可能构成治疗由压力引起的心血管后果的重要药理学策略。