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Role of angiotensin receptors in the medial amygdaloid nucleus in autonomic, baroreflex and cardiovascular changes evoked by chronic stress in rats
European Journal of Neroscience ( IF 3.4 ) Pub Date : 2020-12-29 , DOI: 10.1111/ejn.15094 Willian Costa-Ferreira 1, 2 , Lucas Gomes-de-Souza 1, 2 , Carlos C Crestani 1, 2
European Journal of Neroscience ( IF 3.4 ) Pub Date : 2020-12-29 , DOI: 10.1111/ejn.15094 Willian Costa-Ferreira 1, 2 , Lucas Gomes-de-Souza 1, 2 , Carlos C Crestani 1, 2
Affiliation
This study investigated the role of AT1, AT2 and Mas angiotensinergic receptors within the MeA in autonomic, cardiovascular and baroreflex changes evoked by a 10‐day (1 hr daily) repeated restraint stress (RRS) protocol. Analysis of cardiovascular function after the end of the RRS protocol indicated increased values of arterial pressure, without heart rate changes. Arterial pressure increase was not affected by acute MeA treatment after the RRS with either the selective AT1 receptor antagonist losartan, the selective AT2 receptor antagonist PD123319 or the selective Mas receptor antagonist A‐779. Analysis of heart rate variability indicated that RRS increased the sympathetic tone to the heart, which was inhibited by MeA treatment with either losartan, PD123319 or A‐779. Baroreflex function assessed using the pharmacological approach via intravenous infusion of vasoactive agents revealed a facilitation of tachycardia evoked by blood pressure decrease in chronically stressed animals, which was inhibited by MeA treatment with losartan. Conversely, baroreflex responses during spontaneous fluctuations of blood pressure were impaired by RRS, and this effect was not affected by injection of the angiotensinergic receptor antagonists into the MeA. Altogether, the data reported in the present study suggest an involvement of both angiotensinergic receptors present in the MeA in autonomic imbalance evoked by RRS, as well as an involvement of MeA AT1 receptor in the enhanced baroreflex responses during full range of blood pressure changes. Results also indicate that RRS‐evoked increase in arterial pressure and impairment of baroreflex responses during spontaneous variations of arterial pressure are independent of MeA angiotensinergic receptors.
中文翻译:
内侧杏仁核血管紧张素受体在大鼠慢性应激引起的自主神经、压力反射和心血管变化中的作用
本研究调查了 MeA 内 AT 1、AT 2和 Mas 血管紧张素能受体在 10 天(每天 1 小时)重复约束压力 (RRS) 方案引起的自主神经、心血管和压力反射变化中的作用。RRS 方案结束后的心血管功能分析表明动脉压值增加,心率没有变化。使用选择性 AT 1受体拮抗剂氯沙坦、选择性 AT 2的 RRS 后急性 MeA 治疗不会影响动脉压升高受体拮抗剂 PD123319 或选择性 Mas 受体拮抗剂 A-779。心率变异性分析表明,RRS 增加了心脏的交感神经张力,而氯沙坦、PD123319 或 A-779 的 MeA 治疗可抑制这种张力。使用药理学方法通过静脉输注血管活性剂评估压力反射功能显示,慢性应激动物的血压降低可促进心动过速,而氯沙坦的 MeA 治疗可抑制心动过速。相反,在血压自发波动期间的压力反射反应受到 RRS 的损害,并且这种效应不受将血管紧张素受体拮抗剂注射到 MeA 中的影响。共,1受体在血压全范围变化期间增强的压力反射反应。结果还表明,在动脉压自发变化期间,RRS 诱发的动脉压升高和压力反射反应受损与 MeA 血管紧张素能受体无关。
更新日期:2021-02-15
中文翻译:
内侧杏仁核血管紧张素受体在大鼠慢性应激引起的自主神经、压力反射和心血管变化中的作用
本研究调查了 MeA 内 AT 1、AT 2和 Mas 血管紧张素能受体在 10 天(每天 1 小时)重复约束压力 (RRS) 方案引起的自主神经、心血管和压力反射变化中的作用。RRS 方案结束后的心血管功能分析表明动脉压值增加,心率没有变化。使用选择性 AT 1受体拮抗剂氯沙坦、选择性 AT 2的 RRS 后急性 MeA 治疗不会影响动脉压升高受体拮抗剂 PD123319 或选择性 Mas 受体拮抗剂 A-779。心率变异性分析表明,RRS 增加了心脏的交感神经张力,而氯沙坦、PD123319 或 A-779 的 MeA 治疗可抑制这种张力。使用药理学方法通过静脉输注血管活性剂评估压力反射功能显示,慢性应激动物的血压降低可促进心动过速,而氯沙坦的 MeA 治疗可抑制心动过速。相反,在血压自发波动期间的压力反射反应受到 RRS 的损害,并且这种效应不受将血管紧张素受体拮抗剂注射到 MeA 中的影响。共,1受体在血压全范围变化期间增强的压力反射反应。结果还表明,在动脉压自发变化期间,RRS 诱发的动脉压升高和压力反射反应受损与 MeA 血管紧张素能受体无关。