Expression of Neuronal NO Synthase and the Hyperglycemic Reflex to Anoxic Stimulation of the Carotid Body in Normoglycemic and Hyperglycemic Rats

Blood glucose levels are detected by glucoreceptors located in the central nervous system (CNS) and peripheral tissues, in particular in the pancreatic beta cells and carotid bodies (CBs). Nitric oxide (NO) modulates the chemosensory discharge in the CBs by temporarily inhibiting oxygen (O2) consumption through the blockade of mitochondrial cytochrome-c-oxidase (Cit-c). It has been reported that the NO synthase (NOS) level is higher in hyperglycemic rats. Therefore, there is a possibility that acute anoxia affects the gene expression of neuronal NOS (nNOS) in the CBs, and this is mediated by the glucose level. Male Sprague-Dawley rats (250 to 300 g) anesthetized with sodium pentobarbital (30 mg/kg) and artificially ventilated were used in our experiments. The rats were divided in four groups: i) control 1, normoglycemic rats (C1); ii) experimental 1, normoglycemic rats (E1) with anoxic CB stimulation with cyanide; iii) control 2, hyperglycemic rats (C2) treated as in the C1 group, and iv) experimental 2, hyperglycemic rats (E2) treated as in the E1 group. At the end of the experiment, the blood glucose levels were measured, and the CBs were extirpated to determine nNOS expression through qPCR testing. Anoxic stimulation of the CBs induced a significant increase in the glucose level when the E1 vs. E2 groups were compared, whereas nNOS mRNA expression in E2 rats was smaller when compared to E1. It is concluded that hyperglycemia induced by streptozotocin reduces nNOS mRNA expression in the CBs and hyperglycemic reflex after anoxic stimulation of the CBs in rats.

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