Increased Superoxide Production during Fatigue in the Perfused Rat Diaphragm

Kolbeck, Ralph C.; She, Z. W.; Callahan, Leigh Ann; Nosek, Thomas M.

doi:10.1164/ajrccm.156.1.9610041

Cited by 94 publications

(97 citation statements)

References 30 publications

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“…Our finding suggests that oxidative stress does not contribute to hypoxia-induced functional remodelling in sternohyoid muscle during development. In isolated perfused rat diaphragm, significant increases in superoxide during fatigue were determined by measuring the level of cytochrome c reduction but SOD did not ameliorate diaphragm fatigue [60]. As such, SOD-mimetics may not always be the best approach for protection of skeletal muscle function during oxidative stress (hypoxia).…”

Section: Figurementioning

confidence: 99%

Effects of sustained hypoxia on sternohyoid and diaphragm muscle during development

Carberry

McMorrow

Bradford

et al. 2013

European Respiratory Journal

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Sustained hypoxia is a dominant feature of respiratory disease. Despite the clinical significance, the effects of sustained hypoxia on the form and function of respiratory muscle during development are relatively underexplored.Wistar rats were exposed to 1 week of sustained hypoxia (ambient pressure 450 mmHg) or normoxia at various time points during development. Sternohyoid and diaphragm muscle contractile and endurance properties were assessed in vitro. Muscle succinate dehydrogenase and myosin heavy chain composition were determined. The role of reactive oxygen species in hypoxia-induced muscle remodelling was assessed.Sustained hypoxia increased sternohyoid muscle force and fatigue in early but not late development, effects that persisted after return to normoxia. Hypoxia-induced sternohyoid muscle fatigue was not attributable to fibre type transitions or to a decrease in oxidative capacity. Chronic supplementation with the superoxide scavenger tempol did not prevent hypoxia-induced sternohyoid muscle fatigue, suggesting that mechanisms unrelated to oxidative stress underpin hypoxia-induced maladaptation in sternohyoid muscle. Sustained hypoxia had no effect on diaphragm muscle fatigue.We conclude that there are critical windows during development for hypoxia-induced airway dilator muscle maladaptation. Sustained hypoxia-induced impairment of upper airway muscle endurance may persist into later life. Upper airway muscle dysfunction could have deleterious consequences for the control of pharyngeal airway calibre in vivo. @ERSpublications There are critical windows during development for hypoxia-induced airway dilator muscle maladaptation

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Section: Figurementioning

confidence: 99%

Effects of sustained hypoxia on sternohyoid and diaphragm muscle during development

Carberry

McMorrow

Bradford

et al. 2013

European Respiratory Journal

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“…Reduced nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase activity was quantified by cytochrome c method from the absorbance with or without superoxide dismutase, as described previously. 18,19 …”

Section: Nadph Oxidase Activitymentioning

confidence: 99%

Attenuation of Inflammatory Vascular Remodeling by Angiotensin II Type 1 Receptor–Associated Protein

et al. 2006

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Abstract-To explore the role of angiotensin II Type 1 receptor-associated protein (ATRAP) in vascular remodeling, we developed transgenic mice for mouse ATRAP cDNA and examined remodeling after inflammatory vascular injury induced by polyethylene cuff placement. In ATRAP transgenic (ATRAP-Tg) mice, ATRAP mRNA was increased 3-to 4-fold in the heart, aorta, and femoral artery. ATRAP-Tg mice showed no significant change in body weight, systolic blood pressure, heart rate, and heart/body weight ratio. However, cell proliferation and neointimal formation in the injured artery were attenuated in ATRAP-Tg mice. The increase in NADPH oxidase activity and the expression of p22 phox , a reduced nicotinamide-adenine dinucleotide/reduced nicotinamide-adenine dinucleotide phosphate oxidase subunit, after cuff placement was also attenuated in ATRAP-Tg mice. Moreover, activation of extracellular signal-regulated kinase, signal transducer and activator of transcription 1, and signal transducer and activator of transcription 3 after cuff placement was significantly reduced in ATRAP-Tg mice. Pressor response and cardiac hypertrophy induced by angiotensin II infusion and pressure overload were also attenuated in ATRAP-Tg mice. These results suggest that ATRAP plays an important role in vascular remodeling as a negative regulator. Previous reports indicate that the intracellular carboxylterminal tail of the receptor plays an important role in activation of receptor-coupled G protein and internalization of the AT 1 receptor. [1][2][3][4][5][6] We cloned a novel AT 1 receptorassociated protein (ATRAP) using a yeast 2-hybrid screening system. 7 ATRAP has 3 transmembrane domains and interacts with the intracellular carboxyl-terminal domain of the AT 1 receptor, but it does not interact with the AT 2 receptor, m 3 muscarinic receptor, bradykinin B 2 receptor, endothelin ETB receptor, or ␤ 2 -adrenergic receptor. It is reported that ATRAP modulates AT 1 receptor function in COS-7 cells, human embryonic kidney 293 cells, and cultured mouse cardiomyocytes. Overexpression of ATRAP significantly decreases the number of AT 1 receptors on the cell surface and also decreases the degree of p38 mitogen-activated protein kinase phosphorylation, activity of the c-fos promoter, and protein synthesis on Ang II treatment. [7][8][9] We also reported that overexpression of ATRAP in cultured vascular smooth muscle cells (VSMCs) enhanced internalization of the AT 1 receptor and attenuated DNA synthesis and activation of extracellular signal-regulated kinase (ERK), Akt, and signal transducer and activator of transcription (STAT) induced by Ang II. 10 Polyethylene cuff placement around the femoral artery induces inflammatory vascular injury and remodeling responses accompanied by an increase in AT 1 and AT 2 receptor expression. VSMC proliferation, neointimal formation, inflammatory response, and oxidative stress in vascular injury were significantly attenuated in AT 1 a receptor-deficient mice. [11][12][13] Moreover, administration of an AT 1 receptor bloc...

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“…NADPH oxidase activity was quantified from the absorbance with or without superoxide dismutase, as previously described. 14 …”

Section: Measurement Of Nadph Oxidase Activitymentioning

confidence: 99%

Sex Difference in Vascular Injury and the Vasoprotective Effect of Valsartan Are Related to Differential AT ₂ Receptor Expression

et al. 2005

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Abstract-The angiotensin II type 2 (AT 2 ) receptor is upregulated in pathological conditions such as vascular injury and exerts antagonistic effects against AT 1 receptor-mediated actions. We examined the possibility that the sex difference in vascular remodeling is associated with altered AT 2 receptor expression, which is located on the X chromosome. In this study, we examined this possibility by using AT 2 receptor-null (Agtr2Ϫ) mice. Vascular injury was induced by polyethylene cuff placement around the femoral artery of wild-type (Agtr2ϩ) and Agtr2Ϫ mice. In Agtr2ϩ mice, AT 2 receptor expression in the injured artery was enhanced, and this increase was greater in female than in male mice, with no significant difference in AT 1 receptor expression between male and female mice. Increases in neointimal formation, DNA synthesis, expression of monocyte chemoattractant protein-1, production of superoxide anion, and NADPH oxidase activity in the injured artery were attenuated in female compared with male mice. These parameters were augmented in Agtr2Ϫ mice, whereas the sex differences in these parameters were smaller in Agtr2Ϫ than in Agtr2ϩ mice. Treatment with a nonhypotensive dose of the AT 1 receptor blocker valsartan decreased these parameters significantly in Agtr2ϩ mice, and these inhibitory effects of valsartan were greater in female mice. This sex difference in valsartan's inhibitory effect was less marked in Agtr2Ϫ mice. Our results suggest that the sex difference in response to vascular injury could be at least partially attributed to the exaggerated AT 2 receptor expression in the injured vessel in female mice. Key Words: angiotensin II Ⅲ inflammation Ⅲ oxidative stress Ⅲ receptors, angiotensin Ⅲ remodeling R ecent evidence has revealed that actions of the angiotensin (Ang) II receptor subtypes AT 1 and AT 2 are mutually antagonistic. 1,2 The AT 2 receptor is abundantly and widely expressed in fetal tissues, but its expression declines rapidly after birth. 3,4 Interestingly, the AT 2 receptor is reexpressed in certain pathological conditions such as inflammation and vascular injury. 1,2 These findings suggest that the AT 2 receptor plays an important role not only in vasculogenesis but also in vascular remodeling.The effect of AT 1 receptor blockers (ARBs) may not be entirely due to the blockade of the AT 1 receptor. When the AT 1 receptor is blocked, increased Ang II may act on the AT 2 receptor, which could be involved in the effects of the ARB. The AT 2 receptor plays a role in the pathogenesis of cardiovascular and renal diseases. However, the results, though suggestive, are sometimes equivocal. A more extensive knowledge of the AT 2 receptor could therefore contribute to the understanding of the clinical benefits of ARBs. We have previously reported that the AT 2 receptor exerts antiinflammatory and antiproliferative effects by counteracting the AT 1 receptor in the process of neointimal formation after vascular injury in a mouse model of vascular disease induced by polyethylene cuff placement. 5,...

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Increased Superoxide Production during Fatigue in the Perfused Rat Diaphragm

Cited by 94 publications

References 30 publications

Effects of sustained hypoxia on sternohyoid and diaphragm muscle during development

Effects of sustained hypoxia on sternohyoid and diaphragm muscle during development

Attenuation of Inflammatory Vascular Remodeling by Angiotensin II Type 1 Receptor–Associated Protein

Sex Difference in Vascular Injury and the Vasoprotective Effect of Valsartan Are Related to Differential AT ₂ Receptor Expression

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Increased Superoxide Production during Fatigue in the Perfused Rat Diaphragm

Cited by 94 publications

References 30 publications

Effects of sustained hypoxia on sternohyoid and diaphragm muscle during development

Effects of sustained hypoxia on sternohyoid and diaphragm muscle during development

Attenuation of Inflammatory Vascular Remodeling by Angiotensin II Type 1 Receptor–Associated Protein

Sex Difference in Vascular Injury and the Vasoprotective Effect of Valsartan Are Related to Differential AT 2 Receptor Expression

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Sex Difference in Vascular Injury and the Vasoprotective Effect of Valsartan Are Related to Differential AT ₂ Receptor Expression