Laboratory of Pharmacology, School of Pharmaceutical Sciences, São Paulo State University (UNESP), Rodovia Araraquara-Jaú Km 01 (Campus Universitário), Campus Ville, Araraquara, SP, 14800-903, Brazil.
Joint UFSCar-UNESP Graduate Program in Physiological Sciences, São Carlos, SP, Brazil.
Pflugers Arch. 2019 Sep;471(9):1173-1182. doi: 10.1007/s00424-019-02301-3. Epub 2019 Aug 8.
The medial amygdaloid nucleus (MeA) is a limbic structure that has been demonstrated to be part of the central circuitry regulating baroreflex function. However, the local neurochemical mechanisms involved in baroreflex control by this forebrain structure is poorly understood. Thus, in the present study, we investigated the specific role of AT, AT, and MAS angiotensinergic receptors within the MeA in baroreflex responses in unanesthetized rats. For this, the baroreflex function was assessed using both the pharmacological approach via intravenous infusion of vasoactive agents and the sequence analysis technique. Using the pharmacological approach, we observed that bilateral microinjection of the selective AT receptor antagonist PD123319 into the MeA increased the tachycardia evoked by blood pressure decrease, but without affecting the reflex bradycardia caused by blood pressure increase. Besides, bilateral microinjection of the selective MAS receptor antagonist A-779 decreased both tachycardic and bradycardic responses of the baroreflex. The sequence analysis technique indicated that PD123319 into the MeA increased baroreflex effectiveness index while A-779 had an opposite effect. Treatment of the MeA with the selective AT receptor antagonist losartan did not affect baroreflex function assessed by either the pharmacological approach or sequence analysis technique. Overall, these findings provide evidence that MAS receptor within the MeA plays a facilitatory role in baroreflex function, whereas local AT receptor inhibits cardiac baroreflex responses. Results also indicate that AT receptor within the MeA is not involved in the control of baroreflex function.
内侧杏仁核（MeA）是边缘结构的一部分，已被证明是调节压力反射功能的中枢回路的一部分。然而，该前脑结构参与压力反射控制的局部神经化学机制尚不清楚。因此，在本研究中，我们研究了 MeA 内 AT、AT 和 MAS 血管紧张素能受体在未麻醉大鼠压力反射反应中的特定作用。为此，通过静脉输注血管活性药物和序列分析技术评估了压力反射功能。使用药理学方法，我们观察到选择性 AT 受体拮抗剂 PD123319 双侧微注射到 MeA 中会增加血压下降引起的心动过速，但不会影响血压升高引起的反射性心动过缓。此外，选择性 MAS 受体拮抗剂 A-779 的双侧微注射会降低压力反射的心动过速和心动过缓反应。序列分析技术表明，PD123319 进入 MeA 会增加压力反射有效指数，而 A-779 则有相反的作用。用选择性 AT 受体拮抗剂洛沙坦处理 MeA 不会影响通过药理学方法或序列分析技术评估的压力反射功能。总的来说，这些发现提供了证据，证明 MeA 内的 MAS 受体在压力反射功能中起促进作用，而局部 AT 受体抑制心脏压力反射反应。结果还表明，MeA 内的 AT 受体不参与压力反射功能的控制。
