The bed nucleus of the stria terminalis (BNST) is a forebrain structure, involved in the modulation of neuroendocrine, cardiovascular and autonomic responses. One of the responses is baroreflex activity, which consists in a neural mechanism responsible for keeping the blood pressure within a narrow range of variation. It has been reported that blockade of BNST α₁-adrenoceptors increased the bradycardic component of baroreflex. In addition, such receptors are able to modulate glutamate release in this structure. Interestingly, BNST NMDA receptor antagonism and neuronal nitric oxide synthase (nNOS) inhibition led to the same effect of the α₁-adrenoceptors blockade on baroreflex bradycardic response. Therefore, the hypothesis of the present study is that BNST noradrenergic transmission interacts with NMDA/NO pathway through α₁ adrenoceptors to modulate the baroreflex activity. Male Wistar rats had stainless steel guide cannulas bilaterally implanted in the BNST. Subsequently, a catheter was inserted into the femoral artery for cardiovascular recordings, and into the femoral vein for assessing baroreflex activation. Injection of the noradrenaline reuptake inhibitor reboxetine in the BNST did not modify the tachycardic, but significantly decreased the bradycardic component of baroreflex. Administration of an α₁, but not an α₂ antagonist into the BNST prior to reboxetine prevented this effect. Likewise, previous injection of NMDA/NO pathway blockers inhibited the effect of reboxetine on bradycardic response. In conclusion, it was demonstrated for the first time the existence of an interaction between BNST noradrenergic, glutamatergic and nitrergic neurotransmissions in the modulation of bradycardic baroreflex response.

终纹床核 (BNST) 是一种前脑结构，参与调节神经内分泌、心血管和自主神经反应。反应之一是压力反射活动，它包括负责将血压保持在狭窄变化范围内的神经机制。据报道，阻断 BNST α _{1 -}肾上腺素能受体会增加压力反射的心动过缓成分。此外，此类受体能够调节该结构中的谷氨酸释放。有趣的是，BNST NMDA 受体拮抗作用和神经元一氧化氮合酶 (nNOS) 抑制导致了与 α ₁相同的效果-肾上腺素能受体阻滞压力反射性心动过缓反应。因此，本研究的假设是 BNST 去甲肾上腺素能传递通过 α ₁肾上腺素受体与 NMDA/NO 通路相互作用以调节压力反射活动。雄性 Wistar 大鼠在 BNST 中双侧植入不锈钢导管。随后，将导管插入股动脉进行心血管记录，并插入股静脉以评估压力反射激活。在 BNST 中注射去甲肾上腺素再摄取抑制剂瑞波西汀并没有改变心动过速，但显着降低了压力反射的心动过缓成分。使用 α ₁，但不使用 α ₂在瑞波西汀之前将拮抗剂加入 BNST 阻止了这种作用。同样，之前注射 NMDA/NO 通路阻滞剂会抑制瑞波西汀对心动过缓反应的影响。总之，首次证明了 BNST 去甲肾上腺素能、谷氨酸能和硝能神经传递在调节心动过缓压力反射反应中存在相互作用。