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We demonstrated recently that superoxide anion levels are elevated in prevertebral sympathetic ganglia of deoxycorticosterone acetate-salt hypertensive rats and that this superoxide anion is generated by reduced nicotinamide-adenine dinucleotide phosphate oxidase. In this study we compared the reduced nicotinamide-adenine dinucleotide phosphate oxidase enzyme system of dorsal root ganglion (DRG) and sympathetic celiac ganglion (CG) and its regulation in hypertension. The reduced nicotinamide-adenine dinucleotide phosphate oxidase activity of ganglion extracts was measured using fluorescence spectrometry of dihydroethidine; the activity in hypertensive dorsal root ganglion was 34% lower than in normotensive DRG. In contrast, activity was 79% higher in hypertensive CG than normotensive CG. mRNA for the oxidase subunits NOX1, NOX2, NOX4, p47(phox), and p22(phox) were present in both CG and DRG; mRNA for NOX4 was significantly higher in CG than in DRG. The levels of mRNA and protein expression of the membrane-bound catalytic subunit p22(phox) and of the regulatory subunits p47(phox) and Rac-1 were measured in CG and DRG in normotensive and hypertensive rats. p22(phox) mRNA and protein expression was greater in CG of hypertensive rats but not in DRG. Compared with normotensive controls, p47(phox) mRNA and protein, as well as Rac-1 protein, were significantly decreased in hypertensive DRG but not in CG. Immunohistochemical staining of p47(phox) showed translocation from cytoplasm to membrane in hypertensive CG but not in hypertensive DRG. This suggests that reduced nicotinamide-adenine dinucleotide phosphate oxidase activation in sympathetic neurons and sensory neurons is regulated in opposite directions in hypertension. This differential regulation may contribute to unbalanced vasomotor control and enhanced vasoconstriction in the splanchnic circulation. [ABSTRACT FROM AUTHOR]

The article discusses a study which compared the reduced nicotinamide-adenine dinucleotide phosphate oxidase enzyme system of dorsal root ganglion (DRG) and sympathetic celiac ganglion (CG) and its regulation in hypertension. Fluorescence spectrometry of dihydroethidine was used in the study to measure the reduced nicotinamide-adenine dinucleotide phosphate oxidase activity of ganglion extracts.

Celiac ganglionectomy attenuates the increase in arterial pressure (AP) seen in the DOCA-salt model of hypertension; however, it is unknown which population of neurons in the celiac ganglion (CG) is responsible for this attenuation. Therefore, we ablated sympathetic post ganglionic neurons selectively innervating mesenteric blood vessels by applying a retrograde tracer, cholera toxin subunit b, conjugated to the neurotoxin saporin (CTB-SAP) on multiple, adjacent branches (~6mm) of mesenteric arteries and veins. Control animals received PBS instead of a CTB-SAP treatment. After 7-10 days rats were anesthetized, and fitted with a femoral catheter to record AP. Nicotine (200mM) was then applied to the surface of the surgically-exposed CG, which caused a significant increase in AP in control animals but not in CTB-SAP treated animals (Table 1 ). Quantitative morphometry done on the CG revealed a significant reduction in the density of ganglionic neurons in CTB-SAP treated animals when compared to control animals (Table 1 ). This study shows ablating CG neurons that innervate such a small portion of the mesenteric vasculature reduces the elevation of systemic AP induced by nicotine. Moreover, this study gives way for further investigations into how ablation of neurons innervating mesenteric arteries or veins can modulate AP. [ABSTRACT FROM AUTHOR]

Sympathetic activity is chronically elevated in hypertensive human patients and in many animal models of hypertension, including the deoxycorticosterone (DOCA)-salt rat model. Sympathetic ganglia receive signals from the central nervous system and relay them to blood vessels and peripheral organs. How sympathetic ganglia respond to activation signals differently in hypertension is not fully understood. We examined how direct and indirect activators of sympathetic ganglia would influence neuronal activation. 2-deoxy-D-glucose (2-DG) is a glucose analog that causes hypoglycemia leading to centrally-mediated, indirect activation of celiac ganglia, a prevertebral sympathetic ganglion. Nicotine directly activates sympathetic ganglia by acting on cholinergic receptors found on most sympathetic neurons. Acute neuronal activation was examined by measuring c-fos immunoreactivity (ir). We hypothesized that since there is higher chronic sympathetic activity in DOCA-salt hypertensive than normotensive rats, both direct and indirect acute activators will induce higher c-fos expression in sympathetic ganglia of normotensive than hypertensive rats. Maximal c-fos expression for 2-DG (800mg/kg i.p.) and nicotine (2mg/kg s.c.) treatments was observed 2hrs post-treatment and for all following experiments, celiac ganglia were dissected and fixed 2hrs post-treatment. Following nicotine treatment, c-fos expression was significantly higher in celiac ganglia of normotensive (25.5 ± 9.7 c-fos ir neurons/m^2) than hypertensive (12.0 ± 4.8 c-fos ir neurons/m^2) rats. However, following 2-DG treatment, c-fos expression was similar in celiac ganglia of normotensive (49.1 ± 17.6 c-fos ir neurons/m^2) and hypertensive (49.4 ± 16.0 c-fos ir neurons/m^2). In contrast with our hypothesis, only the direct but not the indirect activation of sympathetic ganglia induced higher sympathetic neuronal activation in normotensive than hypertensive rats. Thus, a centrally-mediated metabolic stimulus does not activate pathways to sympathetic ganglia differentially in normotension versus hypertension. However, direct ganglionic stimulation leads to greater neuronal activation in normotensive than hypertensive ganglia. [ABSTRACT FROM AUTHOR]