author_facet Wang, Gang
Anrather, Josef
Huang, Jie
Speth, Robert C.
Pickel, Virginia M.
Iadecola, Costantino
Wang, Gang
Anrather, Josef
Huang, Jie
Speth, Robert C.
Pickel, Virginia M.
Iadecola, Costantino
author Wang, Gang
Anrather, Josef
Huang, Jie
Speth, Robert C.
Pickel, Virginia M.
Iadecola, Costantino
spellingShingle Wang, Gang
Anrather, Josef
Huang, Jie
Speth, Robert C.
Pickel, Virginia M.
Iadecola, Costantino
The Journal of Neuroscience
NADPH Oxidase Contributes to Angiotensin II Signaling in the Nucleus Tractus Solitarius
General Neuroscience
author_sort wang, gang
spelling Wang, Gang Anrather, Josef Huang, Jie Speth, Robert C. Pickel, Virginia M. Iadecola, Costantino 0270-6474 1529-2401 Society for Neuroscience General Neuroscience http://dx.doi.org/10.1523/jneurosci.1176-04.2004 <jats:p>Angiotensin II (AngII), acting through angiotensin type 1 (AT<jats:sub>1</jats:sub>) receptors, exerts powerful effects on central autonomic networks regulating cardiovascular homeostasis and fluid balance; however, the mechanisms of AngII signaling in functionally defined central autonomic neurons have not been fully elucidated. In vascular cells, reactive oxygen species (ROS) generated by the enzyme NADPH oxidase play a major role in AngII signaling. Thus, we sought to determine whether NADPH oxidase is present in central autonomic neurons and, if so, whether NADPH oxidase-derived ROS are involved in the effects of AngII on these neurons. The present studies focused on the intermediate dorsomedial nucleus of the solitary tract (dmNTS) because this region receives autonomic afferents via the vagus nerve and is an important site of AngII actions. Using double-label immunoelectron microscopy, we found that the essential NADPH oxidase subunit gp91<jats:sup>phox</jats:sup>is present in somatodendric and axonal profiles containing AT<jats:sub>1</jats:sub>receptors. The gp91<jats:sup>phox</jats:sup>-labeled dendrites received inputs from large axon terminals resembling vagal afferents. In parallel experiments using patch clamp of dissociated NTS neurons anterogradely labeled via the vagus, we found that AngII potentiates the L-type Ca<jats:sup>2+</jats:sup>currents, an effect mediated by AT<jats:sub>1</jats:sub>receptors and abolished by the ROS scavenger Mn(III) tetrakis (4-benzoic acid) porphyrin chloride. The NADPH oxidase assembly inhibitor apocynin and the peptide inhibitor gp91<jats:sup>phox</jats:sup>docking sequence, but not its scrambled version, also blocked the potentiation. The results provide evidence that NADPH oxidase-derived ROS are involved in the effects of AngII on Ca<jats:sup>2+</jats:sup>influx in NTS neurons receiving vagal afferents and support the notion that ROS are important signaling molecules in central autonomic networks.</jats:p> NADPH Oxidase Contributes to Angiotensin II Signaling in the Nucleus Tractus Solitarius The Journal of Neuroscience
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title NADPH Oxidase Contributes to Angiotensin II Signaling in the Nucleus Tractus Solitarius
title_unstemmed NADPH Oxidase Contributes to Angiotensin II Signaling in the Nucleus Tractus Solitarius
title_full NADPH Oxidase Contributes to Angiotensin II Signaling in the Nucleus Tractus Solitarius
title_fullStr NADPH Oxidase Contributes to Angiotensin II Signaling in the Nucleus Tractus Solitarius
title_full_unstemmed NADPH Oxidase Contributes to Angiotensin II Signaling in the Nucleus Tractus Solitarius
title_short NADPH Oxidase Contributes to Angiotensin II Signaling in the Nucleus Tractus Solitarius
title_sort nadph oxidase contributes to angiotensin ii signaling in the nucleus tractus solitarius
topic General Neuroscience
url http://dx.doi.org/10.1523/jneurosci.1176-04.2004
publishDate 2004
physical 5516-5524
description <jats:p>Angiotensin II (AngII), acting through angiotensin type 1 (AT<jats:sub>1</jats:sub>) receptors, exerts powerful effects on central autonomic networks regulating cardiovascular homeostasis and fluid balance; however, the mechanisms of AngII signaling in functionally defined central autonomic neurons have not been fully elucidated. In vascular cells, reactive oxygen species (ROS) generated by the enzyme NADPH oxidase play a major role in AngII signaling. Thus, we sought to determine whether NADPH oxidase is present in central autonomic neurons and, if so, whether NADPH oxidase-derived ROS are involved in the effects of AngII on these neurons. The present studies focused on the intermediate dorsomedial nucleus of the solitary tract (dmNTS) because this region receives autonomic afferents via the vagus nerve and is an important site of AngII actions. Using double-label immunoelectron microscopy, we found that the essential NADPH oxidase subunit gp91<jats:sup>phox</jats:sup>is present in somatodendric and axonal profiles containing AT<jats:sub>1</jats:sub>receptors. The gp91<jats:sup>phox</jats:sup>-labeled dendrites received inputs from large axon terminals resembling vagal afferents. In parallel experiments using patch clamp of dissociated NTS neurons anterogradely labeled via the vagus, we found that AngII potentiates the L-type Ca<jats:sup>2+</jats:sup>currents, an effect mediated by AT<jats:sub>1</jats:sub>receptors and abolished by the ROS scavenger Mn(III) tetrakis (4-benzoic acid) porphyrin chloride. The NADPH oxidase assembly inhibitor apocynin and the peptide inhibitor gp91<jats:sup>phox</jats:sup>docking sequence, but not its scrambled version, also blocked the potentiation. The results provide evidence that NADPH oxidase-derived ROS are involved in the effects of AngII on Ca<jats:sup>2+</jats:sup>influx in NTS neurons receiving vagal afferents and support the notion that ROS are important signaling molecules in central autonomic networks.</jats:p>
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author Wang, Gang, Anrather, Josef, Huang, Jie, Speth, Robert C., Pickel, Virginia M., Iadecola, Costantino
author_facet Wang, Gang, Anrather, Josef, Huang, Jie, Speth, Robert C., Pickel, Virginia M., Iadecola, Costantino, Wang, Gang, Anrather, Josef, Huang, Jie, Speth, Robert C., Pickel, Virginia M., Iadecola, Costantino
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container_title The Journal of Neuroscience
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description <jats:p>Angiotensin II (AngII), acting through angiotensin type 1 (AT<jats:sub>1</jats:sub>) receptors, exerts powerful effects on central autonomic networks regulating cardiovascular homeostasis and fluid balance; however, the mechanisms of AngII signaling in functionally defined central autonomic neurons have not been fully elucidated. In vascular cells, reactive oxygen species (ROS) generated by the enzyme NADPH oxidase play a major role in AngII signaling. Thus, we sought to determine whether NADPH oxidase is present in central autonomic neurons and, if so, whether NADPH oxidase-derived ROS are involved in the effects of AngII on these neurons. The present studies focused on the intermediate dorsomedial nucleus of the solitary tract (dmNTS) because this region receives autonomic afferents via the vagus nerve and is an important site of AngII actions. Using double-label immunoelectron microscopy, we found that the essential NADPH oxidase subunit gp91<jats:sup>phox</jats:sup>is present in somatodendric and axonal profiles containing AT<jats:sub>1</jats:sub>receptors. The gp91<jats:sup>phox</jats:sup>-labeled dendrites received inputs from large axon terminals resembling vagal afferents. In parallel experiments using patch clamp of dissociated NTS neurons anterogradely labeled via the vagus, we found that AngII potentiates the L-type Ca<jats:sup>2+</jats:sup>currents, an effect mediated by AT<jats:sub>1</jats:sub>receptors and abolished by the ROS scavenger Mn(III) tetrakis (4-benzoic acid) porphyrin chloride. The NADPH oxidase assembly inhibitor apocynin and the peptide inhibitor gp91<jats:sup>phox</jats:sup>docking sequence, but not its scrambled version, also blocked the potentiation. The results provide evidence that NADPH oxidase-derived ROS are involved in the effects of AngII on Ca<jats:sup>2+</jats:sup>influx in NTS neurons receiving vagal afferents and support the notion that ROS are important signaling molecules in central autonomic networks.</jats:p>
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spelling Wang, Gang Anrather, Josef Huang, Jie Speth, Robert C. Pickel, Virginia M. Iadecola, Costantino 0270-6474 1529-2401 Society for Neuroscience General Neuroscience http://dx.doi.org/10.1523/jneurosci.1176-04.2004 <jats:p>Angiotensin II (AngII), acting through angiotensin type 1 (AT<jats:sub>1</jats:sub>) receptors, exerts powerful effects on central autonomic networks regulating cardiovascular homeostasis and fluid balance; however, the mechanisms of AngII signaling in functionally defined central autonomic neurons have not been fully elucidated. In vascular cells, reactive oxygen species (ROS) generated by the enzyme NADPH oxidase play a major role in AngII signaling. Thus, we sought to determine whether NADPH oxidase is present in central autonomic neurons and, if so, whether NADPH oxidase-derived ROS are involved in the effects of AngII on these neurons. The present studies focused on the intermediate dorsomedial nucleus of the solitary tract (dmNTS) because this region receives autonomic afferents via the vagus nerve and is an important site of AngII actions. Using double-label immunoelectron microscopy, we found that the essential NADPH oxidase subunit gp91<jats:sup>phox</jats:sup>is present in somatodendric and axonal profiles containing AT<jats:sub>1</jats:sub>receptors. The gp91<jats:sup>phox</jats:sup>-labeled dendrites received inputs from large axon terminals resembling vagal afferents. In parallel experiments using patch clamp of dissociated NTS neurons anterogradely labeled via the vagus, we found that AngII potentiates the L-type Ca<jats:sup>2+</jats:sup>currents, an effect mediated by AT<jats:sub>1</jats:sub>receptors and abolished by the ROS scavenger Mn(III) tetrakis (4-benzoic acid) porphyrin chloride. The NADPH oxidase assembly inhibitor apocynin and the peptide inhibitor gp91<jats:sup>phox</jats:sup>docking sequence, but not its scrambled version, also blocked the potentiation. The results provide evidence that NADPH oxidase-derived ROS are involved in the effects of AngII on Ca<jats:sup>2+</jats:sup>influx in NTS neurons receiving vagal afferents and support the notion that ROS are important signaling molecules in central autonomic networks.</jats:p> NADPH Oxidase Contributes to Angiotensin II Signaling in the Nucleus Tractus Solitarius The Journal of Neuroscience
spellingShingle Wang, Gang, Anrather, Josef, Huang, Jie, Speth, Robert C., Pickel, Virginia M., Iadecola, Costantino, The Journal of Neuroscience, NADPH Oxidase Contributes to Angiotensin II Signaling in the Nucleus Tractus Solitarius, General Neuroscience
title NADPH Oxidase Contributes to Angiotensin II Signaling in the Nucleus Tractus Solitarius
title_full NADPH Oxidase Contributes to Angiotensin II Signaling in the Nucleus Tractus Solitarius
title_fullStr NADPH Oxidase Contributes to Angiotensin II Signaling in the Nucleus Tractus Solitarius
title_full_unstemmed NADPH Oxidase Contributes to Angiotensin II Signaling in the Nucleus Tractus Solitarius
title_short NADPH Oxidase Contributes to Angiotensin II Signaling in the Nucleus Tractus Solitarius
title_sort nadph oxidase contributes to angiotensin ii signaling in the nucleus tractus solitarius
title_unstemmed NADPH Oxidase Contributes to Angiotensin II Signaling in the Nucleus Tractus Solitarius
topic General Neuroscience
url http://dx.doi.org/10.1523/jneurosci.1176-04.2004