Centro Universitario de Investigaciones Biomédicas, Universidad de Colima, Ave. 25 de Julio s/n, Colima 28045, Mexico; Facultad de Medicina, Universidad de Colima, Ave. 25 de Julio s/n, Colima 28045, Mexico.
Centro Universitario de Investigaciones Biomédicas, Universidad de Colima, Ave. 25 de Julio s/n, Colima 28045, Mexico.
Nitric Oxide. 2014 Jan 30;36:87-93. doi: 10.1016/j.niox.2013.12.004. Epub 2013 Dec 12.
Carotid body chemoreceptors function as glucose sensors and contribute to glucose homeostasis. The nucleus tractus solitarii (NTS) is the first central nervous system (CNS) nuclei for processing of information arising in the carotid body. Here, we microinjected a nitric oxide (NO) donor sodium nitroprusside (SNP), an NO-independent activator of the soluble guanylyl cyclase (sGC) (YC₁) or an NO-synthase (NOS) inhibitor Nω-nitro-l-arginine methyl ester (L-NAME) into the commissural NTS (cNTS) before carotid chemoreceptor anoxic stimulation and measured arterial glucose and the expression of Fos-like immunoreactivity (Fos-ir). Male Wistar rats (250-300 g) were anesthetized, and the carotid sinus was vascularly isolated. Either artificial cerebrospinal fluid (aCSF), SNP, YC₁ or L-NAME were stereotaxically injected into the cNTS. The SNP and YC₁ infused into the cNTS before carotid chemoreceptor stimulation (SNP-2 and YC₁-2 groups) similarly increased arterial glucose compared to the aCSF-2 group. By contrast, infusion of L-NAME into the cNTS before carotid chemoreceptor stimulation (L-NAME-2 group) decreased arterial glucose concentration. The number of cNTS Fos-ir neurons, determined in all the groups studied except for YC₁ groups, significantly increased in SNP-2 rat when compared to the aCSF-2 or SNP-2 groups. Our findings demonstrate that NO signaling, and the correlative activation of groups of cNTS neurons, plays key roles in the hyperglycemic reflex initiated by carotid chemoreceptor stimulation.
颈动脉体化学感受器作为葡萄糖感受器，有助于葡萄糖稳态。孤束核（NTS）是处理颈动脉体产生信息的第一个中枢神经系统（CNS）核。在这里，我们在颈动脉体化学感受器缺氧刺激前将一氧化氮（NO）供体硝普钠（SNP）、NO 非依赖性可溶性鸟苷酸环化酶（sGC）激活剂（YC₁）或一氧化氮合酶（NOS）抑制剂 Nω-硝基-L-精氨酸甲酯（L-NAME）微注射到连合孤束核（cNTS）中，并测量动脉血糖和 Fos 样免疫反应性（Fos-ir）的表达。雄性 Wistar 大鼠（250-300g）麻醉后，血管分离颈动脉窦。立体定向将人工脑脊液（aCSF）、SNP、YC₁或 L-NAME 注入 cNTS。在颈动脉体化学感受器刺激前将 SNP 或 YC₁注入 cNTS（SNP-2 和 YC₁-2 组），与 aCSF-2 组相比，动脉血糖相似增加。相比之下，在颈动脉体化学感受器刺激前将 L-NAME 注入 cNTS（L-NAME-2 组）会降低动脉血糖浓度。除了 YC₁ 组外，在所有研究组的大鼠中，cNTS Fos-ir 神经元的数量都显著增加，与 aCSF-2 或 SNP-2 组相比，SNP-2 大鼠的 cNTS Fos-ir 神经元数量显著增加。我们的研究结果表明，NO 信号转导和相关的 cNTS 神经元群的激活，在颈动脉体化学感受器刺激引发的高血糖反射中发挥关键作用。
