scholarly journals Endothelinergic Contractile Hyperreactivity in Rat Contralateral Carotid to Balloon Injury: Integrated Role for ETB Receptors and Superoxide Anion

2017 ◽  
Vol 2017 ◽  
pp. 1-13
Author(s):  
Larissa Pernomian ◽  
Lilian R. Gimenes ◽  
Mayara S. Gomes ◽  
Bruno N. do Vale ◽  
Cristina R. B. Cardoso ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Superoxide Anion ◽  
Calcium Mobilization ◽  
Balloon Injury ◽  
Superoxide Generation ◽  
Response Curves ◽  
Endothelin 1 ◽  
Functional Assays ◽  
Superoxide Dismutase Mimic ◽  
Lucigenin Chemiluminescence

Temporal consequences of neurocompensation to balloon injury on endothelinergic functionality in rat contralateral carotid were evaluated. Rats underwent balloon injury in left carotid and were treated with CP-96345 (NK1 antagonist). Concentration-response curves for endothelin-1 were obtained in contralateral (right) carotid at 2, 8, 16, 30, or 45 days after surgery in the absence or presence of BQ-123 (ETA antagonist), BQ-788 (ETB antagonist), or Tempol (superoxide-dismutase mimic). Endothelin-1-induced calcium mobilization was evaluated in functional assays carried out with BQ-123, BQ-788, or Tempol. Endothelin-1-induced NADPH oxidase-driven superoxide generation was measured by lucigenin chemiluminescence assays performed with BQ-123 or BQ-788. Endothelin-1-induced contraction was increased in contralateral carotid from the sixteenth day after surgery. This response was restored in CP-96345-treated rats. Endothelium removal or BQ-123 did not change endothelin-1-induced contraction in contralateral carotid. This response was restored by BQ-788 or Tempol. Contralateral carotid exhibited an increased endothelin-1-induced calcium mobilization, which was restored by BQ-788 or Tempol. Contralateral carotid exhibited an increased endothelin-1-induced lucigenin chemiluminescence, which was restored by BQ-788. We conclude that the NK1-mediated neurocompensatory response to balloon injury elicits a contractile hyperreactivity to endothelin-1 in rat contralateral carotid by enhancing the muscular ETB-mediated NADPH oxidase-driven generation of superoxide, which activates calcium channels.

scholarly journals Endothelium-specific activation of NAD(P)H oxidase in aortas of exogenously hyperinsulinemic rats

1999 ◽  
Vol 277 (6) ◽  
pp. E976-E983 ◽  
Author(s):  
Atsunori Kashiwagi ◽  
Kazuya Shinozaki ◽  
Yoshihiko Nishio ◽  
Hiroshi Maegawa ◽  
Yasuhiro Maeno ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Nadph Oxidase ◽  
Superoxide Anion ◽  
Chemiluminescence Method ◽  
Insulin Effect ◽  
Vascular Tissues ◽  
Text Production ◽  
Lucigenin Chemiluminescence

To examine the effects of chronic hyperinsulinemia on vascular tissues, we examined the production of superoxide anion ([Formula: see text]) in the aortic tissues of control and exogenously hyperinsulinemic rats performed by the implantation of an insulin pellet for 4 wk. [Formula: see text]production by aortic segments from hyperinsulinemic rats was 2.4-fold (lucigenin chemiluminescence method) and 1.7-fold (cytochrome c method) of that of control rats without any differences in [Formula: see text]degrading activities in aortic tissues, respectively ( P < 0.025). The increment was completely abolished in the presence of either 100 μmol/l apocynin (an inhibitor of NADPH oxidase) or 10 μmol/l diphenyleneiodonium (an inhibitor of flavin-containing enzyme) and was exclusively endothelium dependent. Consistently, NAD(P)H oxidase activities in endothelial homogenate in hyperinsulinemic rats were dose dependently stimulated above the values of control rats, although these activities in nonendothelial homogenate were not significantly stimulated by insulin. Furthermore, an insulin effect was also demonstrated 1 h after exposing aortic tissues to insulin. These results indicate that[Formula: see text] production specifically increases in endothelium of aortic tissues in chronic hyperinsulinemic rats through the activation of NAD(P)H oxidase.

scholarly journals Inhibition of NADPH oxidase improves impaired reactivity of pial arterioles during chronic exposure to nicotine

2006 ◽  
Vol 100 (2) ◽  
pp. 631-636 ◽  
Author(s):  
Qin Fang ◽  
Hong Sun ◽  
Denise M. Arrick ◽  
William G. Mayhan
Keyword(s):  
Nadph Oxidase ◽  
Superoxide Anion ◽  
Chronic Exposure ◽  
Potential Role ◽  
Osmotic Minipump ◽  
Pial Arterioles ◽  
Cerebral Vasodilatation ◽  
Oxide Synthase ◽  
Lucigenin Chemiluminescence

Our goals were to determine whether chronic exposure to nicotine alters nitric oxide synthase (NOS)-dependent reactivity of cerebral (pial) arterioles and to identify a potential role for NADPH oxidase in impaired NOS-dependent responses during chronic exposure to nicotine. We measured in vivo diameter of pial arterioles to NOS-dependent (acetylcholine and ADP) and -independent (nitroglycerin) agonists in saline-treated rats and rats chronically treated with nicotine (2 mg·kg−1·day−1 for 2 wk via an osmotic minipump). We found that NOS-dependent, but not -independent, vasodilatation was impaired in nicotine-treated compared with saline-treated rats. In addition, the production of superoxide anion (lucigenin chemiluminescence) was increased in rats treated with nicotine compared with saline-treated rats. Furthermore, using Western blot analysis, we found that chronic exposure to nicotine increased p47phox protein in the parietal cortex. Finally, we found that apocynin (40 mg·kg−1·day−1) in the drinking water to inhibit NADPH oxidase alleviated impaired NOS-dependent cerebral vasodilatation in nicotine treated rats but did not alter NOS-dependent responses in saline treated rats and did not alter NOS-independent reactivity in saline- or nicotine-treated rats. These findings suggest that chronic exposure to nicotine impairs NOS-dependent dilatation of pial arterioles by a mechanism that appears to be related to the formation of superoxide anion via activation of NADPH oxidase.

Cadmium decreased superoxide anion derived from NADPH oxidase through overload of calcium in wheat seedling

2020 ◽  
Vol 52 (5) ◽  
Author(s):  
Hongjuan Jiang ◽  
Yi Fu ◽  
Cuixiang Li ◽  
Mengying Chen ◽  
Zewei Gu ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Superoxide Anion ◽  
Wheat Seedling

Grape pomace enzymatic extract restores vascular dysfunction evoked by endothelin-1 and DETCA via NADPH oxidase downregulation and SOD activation

2013 ◽  
Vol 5 (4) ◽  
pp. 1673-1683 ◽  
Author(s):  
Cristina Perez-Ternero ◽  
Rosalia Rodriguez-Rodriguez ◽  
Juan Parrado ◽  
Maria Alvarez de Sotomayor
Keyword(s):  
Nadph Oxidase ◽  
Vascular Dysfunction ◽  
Grape Pomace ◽  
Enzymatic Extract ◽  
Endothelin 1

Topics in Chronic Granulomatous Disease

PEDIATRICS ◽  
1991 ◽  
Vol 88 (1) ◽  
pp. 183-185
Author(s):  
SHIGENOBU UMEKI
Keyword(s):  
Nadph Oxidase ◽  
Chronic Granulomatous Disease ◽  
Host Defense ◽  
Superoxide Anion ◽  
Fungal Infections ◽  
Regulatory Elements ◽  
Granulomatous Disease ◽  
Phagocytic Cells ◽  
Oxidase System ◽  
Membrane Bound

To the Editor.— Such phagocytic cells as neutrophils and macrophages are crucial elements in the host defense against bacterial [See table in the PDF file] and fungal infections. Microbicidal activity depends to a large extent on NADPH oxidase system, which can be activated by stimuli (bacteria, fungi) and which generates the superoxide anion and other highly reactive forms of reduced oxygen.1,2 The neutrophil NADPH oxidase system is composed functionally of membrane-bound catalytic components (which consist of at least two constituents, the low potential cytochrome b5583-5 and flavoprotein5) and soluble cytosolic components6,7 which participate as either catalytic or regulatory elements.

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