ArticleAmerican journal of physiology. Cell physiology2010
Mitochondria-produced superoxide mediates angiotensin II-induced inhibition of neuronal potassium current.
Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 58 citations in OpenAlex.
- Review
- Plasma Angiotensin II Is Increased in Critical Coronavirus Disease 2019.Frontiers in cardiovascular medicine · 2022Article
- Modulations of Cardiac Functions and Pathogenesis by Reactive Oxygen Species and Natural Antioxidants.Antioxidants (Basel, Switzerland) · 2021Review
- Oxidative Stress and Hypertension.Circulation research · 2021Review
- Kinin B1 Receptor Blockade Prevents Angiotensin II-induced Neuroinflammation and Oxidative Stress in Primary Hypothalamic Neurons.Cellular and molecular neurobiology · 2020Article
- ACE-Triggered Hypertension Incites Stroke: Genetic, Molecular, and Therapeutic Aspects.Neuromolecular medicine · 2020Review
- Redox-sensitive calcium/calmodulin-dependent protein kinase IIα in angiotensin II intra-neuronal signaling and hypertension.Redox biology · 2019Article
- Cellular and Molecular Mechanisms Underlying Arterial Baroreceptor Remodeling in Cardiovascular Diseases and Diabetes.Neuroscience bulletin · 2019Review
- A-type KAmerican journal of physiology. Heart and circulatory physiology · 2017Article
- Central TrkB blockade attenuates ICV angiotensin II-hypertension and sympathetic nerve activity in male Sprague-Dawley rats.Autonomic neuroscience : basic & clinical · 2017Article
- Increased mitochondrial superoxide in the brain, but not periphery, sensitizes mice to angiotensin II-mediated hypertension.Redox biology · 2017Article
- Overexpression of Human SOD1 Leads to Discrete Defects in the Cerebellar Architecture in the Mouse.Frontiers in neuroanatomy · 2017Article
- Cross talk between AT1 receptors and Toll-like receptor 4 in microglia contributes to angiotensin II-derived ROS production in the hypothalamic paraventricular nucleus.American journal of physiology. Heart and circulatory physiology · 2016Article
- BDNF contributes to angiotensin II-mediated reductions in peak voltage-gated K+ current in cultured CATH.a cells.Physiological reports · 2015Article
- Rapid metabolism of exogenous angiotensin II by catecholaminergic neuronal cells in culture media.Physiological reports · 2015Article
- Angiotensin II-superoxide-NFκB signaling and aortic baroreceptor dysfunction in chronic heart failure.Frontiers in neuroscience · 2015Review
- Central command dysfunction in rats with heart failure is mediated by brain oxidative stress and normalized by exercise training.The Journal of physiology · 2014Article
- Neuronal uptake of nanoformulated superoxide dismutase and attenuation of angiotensin II-dependent hypertension after central administration.Free radical biology & medicine · 2014Article
- Sensory nerve terminal mitochondrial dysfunction induces hyperexcitability in airway nociceptors via protein kinase C.Molecular pharmacology · 2014Article
- Mitochondrial redox signaling: Interaction of mitochondrial reactive oxygen species with other sources of oxidative stress.Antioxidants & redox signaling · 2014Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Reactive oxygen species (ROS), particularly superoxide (O(2)(.-)), have been identified as key signaling intermediates in ANG II-induced neuronal activation and sympathoexcitation associated with cardiovascular diseases, such as hypertension and heart failure. Studies of the central nervous system have identified NADPH oxidase as a primary source of O(2)(.-) in ANG II-stimulated neurons; however, additional sources of O(2)(.-), including mitochondria, have been mostly overlooked. Here, we tested the hypothesis that ANG II increases mitochondria-produced O(2)(.-) in neurons and that increased scavenging of mitochondria-produced O(2)(.-) attenuates ANG II-dependent intraneuronal signaling. Stimulation of catecholaminergic (CATH.a) neurons with ANG II (100 nM) increased mitochondria-localized O(2)(.-) levels, as measured by MitoSOX Red fluorescence. This response was significantly attenuated in neurons overexpressing the mitochondria-targeted O(2)(.-)-scavenging enzyme Mn-SOD. To examine the biological significance of the ANG II-mediated increase in mitochondria-produced O(2)(.-), we used the whole cell configuration of the patch-clamp technique to record the well-characterized ANG II-induced inhibition of voltage-gated K(+) current (I(Kv)) in neurons. Adenovirus-mediated Mn-SOD overexpression or pretreatment with the cell-permeable antioxidant tempol (1 mM) significantly attenuated ANG II-induced inhibition of I(Kv). In contrast, pretreatment with extracellular SOD protein (400 U/ml) had no effect. Mn-SOD overexpression also inhibited ANG II-induced activation of Ca(2+)/calmodulin kinase II, a redox-sensitive protein known to modulate I(Kv). These data indicate that ANG II increases mitochondrial O(2)(.-), which mediates, at least in part, ANG II-induced activation of Ca(2+)/calmodulin kinase II and inhibition of I(Kv) in neurons.
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