Superoxide anion is elevated in sympathetic neurons in DOCA-salt hypertension via activation of NADPH oxidase

Dai, Xiaoling; Chen, Xian; Kreulen, David L.

doi:10.1152/ajpheart.00052.2005

Cited by 32 publications

(33 citation statements)

References 54 publications

(62 reference statements)

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“…24 Moreover, in sympathetic neurons in DOCA salt-hypertensive rats, superoxide anions were elevated via the activation of NADPH oxidase. 25 Thus, NADPH oxidase may play an important role in ROS production in the brain, and our data are compatible with the other reports. In addition, gp91 phox mRNA expression was elevated in the hypothalamus of DSs compared with that of DRs, even without salt loading, although NADPH oxidase activity was not different.…”

Section: Discussionsupporting

confidence: 93%

Sympathoexcitation by Oxidative Stress in the Brain Mediates Arterial Pressure Elevation in Salt-Sensitive Hypertension

et al. 2007

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Abstract-Central sympathoexcitation is involved in the pathogenesis of salt-sensitive hypertension. We have suggested that oxidative stress in the brain modulates the sympathetic regulation of arterial pressure. Thus, we investigated whether oxidative stress could mediate central sympathoexcitation in salt-sensitive hypertension. Five-to 6-week-old male Dahl salt-sensitive rats and salt-resistant rats were fed with a normal (0.3%) or high-(8%) salt diet for 4 weeks. In urethane-anesthetized and artificially ventilated rats, arterial pressure, renal sympathetic nerve activity, and heart rate decreased in a dose-dependent fashion, when 20 or 40 mol of tempol, a membrane-permeable superoxide dismutase mimetic, was infused into the lateral cerebral ventricle. The same degree of reduction was noted in salt-sensitive and salt-resistant rats without salt loading. Salt loading significantly increased central tempol-induced reductions in arterial pressure (Ϫ29.1Ϯ4.8% versus Ϫ10.6Ϯ3.3% at 40 mol; PϽ0.01), sympathetic nerve activity (Ϫ18.7Ϯ2.0% versus Ϫ7.1Ϯ1.8%; PϽ0.01), and heart rate (Ϫ10.7Ϯ2.8% versus Ϫ2.0Ϯ0.7%; PϽ0.05) in salt-sensitive rats but not in salt-resistant rats. Intracerebroventricular diphenyleneiodonium, a reduced nicotinamide-adenine dinucleotide phosphate oxidase inhibitor, also elicited significantly greater reduction in each parameter in salt-loaded salt-sensitive rats. Moreover, salt loading increased reduced nicotinamide-adenine dinucleotide phosphate-dependent superoxide production in the hypothalamus in salt-sensitive rats but not in salt-resistant rats. In addition, reduced nicotinamide-adenine dinucleotide phosphate oxidase subunits p22 phox , p47 phox , and gp91 phox mRNA expression significantly increased in the hypothalamus of salt-loaded salt-sensitive rats. In conclusion, in salt-sensitive hypertension, increased oxidative stress in the brain, possibly via activation of reduced nicotinamide-adenine dinucleotide phosphate oxidase, may elevate arterial pressure through central sympathoexcitation. Key Words: salt-sensitive hypertension Ⅲ oxidative stress Ⅲ brain Ⅲ hypertension Ⅲ salt Ⅲ sympathetic nervous system Ⅲ Dahl rat S ubstantial findings indicate that abnormal modulation of the sympathetic nervous system may be involved in salt-induced development of hypertension in humans 1 and animals. [2][3][4][5][6] In our previous study, 2 salt loading impaired the arterial baroreceptor reflex associated with abnormal central properties in spontaneously hypertensive rats (SHRs); the sympathetic nerve activity (SNA) was less inhibited by stimulation of the aortic depressor nerve in salt-loaded SHRs. However, salt loading did not affect the SNA in Wistar-Kyoto rats. Similarly, the SNA was augmented with salt loading in Dahl salt-sensitive rats (DSs), but not in Dahl salt-resistant rats (DRs). 3 Intracerebroventricular (ICV) infusion of sodium caused sympathoexcitatory and pressor responses to a greater degree in DSs than in DRs. 4 Thus, central sympathetic activation may be involved in salt-sensitive ...

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Section: Discussionsupporting

confidence: 93%

Sympathoexcitation by Oxidative Stress in the Brain Mediates Arterial Pressure Elevation in Salt-Sensitive Hypertension

et al. 2007

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“…[53][54][55][56][57][58][59][60][61][62] Although neuronal NADPH oxidase activity is never as intense as that expressed by activated microglia, it can have a sufficient impact on neural redox status to influence the function and survival of neurons. Thus, activation of NADPH oxidase in sympathetic neurons is an obligate mediator of the apoptosis evoked by nerve growth factor withdrawal.…”

Section: Nadph Oxidase In Neurons Is Potentially Pathogenicmentioning

confidence: 99%

Oral phycocyanobilin may diminish the pathogenicity of activated brain microglia in neurodegenerative disorders

2010

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“…Meanwhile, the NADPH oxidase activity in HT CGs is 78.6% higher than NT CGs (PϽ0.05 versus NT; nϭ6). 27 p22 phox and p47 phox mRNA were both present in DRGs and CGs as shown above, and these subunits are critical in Figure 2. NADPH oxidase activity is lower in DRGs from DOCAsalt HT rats than from NT control rats but is higher in HT CGs than NT CGs.…”

Section: Nadph Oxidase Activity In Drgs and Cgs In Nt And Ht Ratsmentioning

confidence: 60%

“…PCR products from CG ganglia were consistent with our previous findings in dissociated CG neurons. 27 However, DRG NOX4 mRNA was barely detectable on the regular PCR gel compared with CG. qPCR was then performed to determine the relative expression levels of NOX4 in normal DRGs and CGs.…”

Section: Expression Of Nadph Oxidase Mrna In Normal Rat Drg and Cgmentioning

confidence: 93%

“…27 Freshly prepared ganglia homogenates were incubated with dihydroethidine (10 mol/L), salmon testes DNA (0.5 mg/mL), and the substrate for NADPH oxidase, ␤-NADPH (0.1 mmol/L), for 30 minutes at 37°C in a dark chamber before measuring fluorescence (excitation: 485Ϯ40 nm; emission: 590Ϯ35 nm) with a fluorescence plate reader. A parallel control group was analyzed in each run with no …”

Section: Measurement Of Nadph Oxidase Activitymentioning

confidence: 99%

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Differential Regulation of NADPH Oxidase in Sympathetic and Sensory Ganglia in Deoxycorticosterone Acetate–Salt Hypertension

et al. 2007

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Abstract-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 nicotinamideadenine 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. Key Words: superoxide Ⅲ sympathetic ganglia Ⅲ sensory ganglia Ⅲ NADPH oxidase Ⅲ rat Ⅲ hypertension T he splanchnic circulation is of great importance in regulating systemic blood pressure. It receives Ϸ60% of the cardiac output and contains approximately one third of the total blood volume. 1 The splanchnic circulation is innervated by both the sympathetic division of the autonomic nervous system (prevertebral sympathetic ganglion neurons, including celiac ganglia [CGs] and superior and inferior mesenteric ganglia) and by spinal sensory nerves (dorsal root ganglia neurons [DRGs]). Elevated sympathetic nervous system activation has been shown in various types of hypertension. 2,3 In particular, sympathetic ganglionic blockade can reduce the arterial blood pressure increase in deoxycorticosterone acetate (DOCA)-salt hypertension, 4 indicating an important role of sympathetic ganglia in the development and maintenance of salt-induced hypertension. On the other hand, sensory nerves play a counterregulatory role in preventing increases in blood pressure through either afferent baroreceptormediated mechanisms 5 or efferent release of vasodilatory neuropeptides, such as ...

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Superoxide anion is elevated in sympathetic neurons in DOCA-salt hypertension via activation of NADPH oxidase

Cited by 32 publications

References 54 publications

Sympathoexcitation by Oxidative Stress in the Brain Mediates Arterial Pressure Elevation in Salt-Sensitive Hypertension

Sympathoexcitation by Oxidative Stress in the Brain Mediates Arterial Pressure Elevation in Salt-Sensitive Hypertension

Oral phycocyanobilin may diminish the pathogenicity of activated brain microglia in neurodegenerative disorders

Differential Regulation of NADPH Oxidase in Sympathetic and Sensory Ganglia in Deoxycorticosterone Acetate–Salt Hypertension

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