Insular cortex is a brain structure involved in the modulation of autonomic activity and cardiovascular function. The nitric oxide/cyclic guanosine-3′,5′-monophosphate pathway is a prominent signaling mechanism in the central nervous system, controlling behavioral and physiological responses. Nevertheless, despite evidence regarding the presence of nitric oxide-synthesizing neurons in the insular cortex, its role in the control of autonomic and cardiovascular function has never been reported. Thus, the present study aimed to investigate the involvement of nitric oxide/cyclic guanosine-3′,5′-monophosphate pathway mediated by neuronal nitric oxide synthase (nNOS) activation within the insular cortex in the modulation of baroreflex responses in unanesthetized rats. For this, we evaluated the effect of bilateral microinjection of either the nitric oxide scavenger carboxy-PTIO, the selective neuronal nitric oxide synthase inhibitor N^ω-Propyl-l-arginine or the soluble guanylate cyclase inhibitor ODQ into the insular cortex on the bradycardia evoked by blood pressure increases in response to intravenous infusion of phenylephrine, and the tachycardia caused by blood pressure decreases evoked by intravenous infusion of sodium nitroprusside. Bilateral microinjection of either NPLA or carboxy-PTIO into the insular cortex increased the reflex bradycardic response, whereas the reflex tachycardia was decreased by these treatments. Bilateral microinjection of the soluble guanylate cyclase inhibitor into the insular cortex did not affect any parameter of baroreflex function evaluated. Overall, our findings provide evidence that insular cortex nitrergic signaling, acting via neuronal nitric oxide synthase, plays a prominent role in control of baroreflex function. However, control of reflex responses seems to be independent of soluble guanylate cyclase activation.

岛叶皮层是一种参与调节自主神经活动和心血管功能的大脑结构。一氧化氮/环鸟苷-3',5'-单磷酸途径是中枢神经系统中的重要信号机制，控制行为和生理反应。然而，尽管有证据表明岛叶皮层中存在一氧化氮合成神经元，但从未报道过其在控制自主神经和心血管功能方面的作用。因此，本研究旨在调查由岛叶皮层内神经元一氧化氮合酶 (nNOS) 激活介导的一氧化氮/环鸟苷-3',5'-单磷酸途径在未麻醉大鼠压力反射反应的调节中的参与。为了这，^ω-丙基-lβ-精氨酸或可溶性鸟苷酸环化酶抑制剂ODQ进入岛叶皮层时，静脉滴注苯肾上腺素引起的心动过缓引起血压升高，静脉滴注硝普钠引起血压降低引起的心动过速。将 NPLA 或羧基-PTIO 双侧显微注射到岛叶皮质增加了反射性心动过缓反应，而这些治疗降低了反射性心动过速。将可溶性鸟苷酸环化酶抑制剂双侧显微注射到岛叶皮层不影响评估的压力反射功能的任何参数。总体而言，我们的研究结果提供证据表明，通过神经元一氧化氮合酶作用的岛叶皮层氮能信号在控制压力反射功能方面起着重要作用。然而，