| Name | angiotensin II |
|---|---|
| Synonyms | AGT; ANG II; ANHU; Angiotensin I; Angiotensin II; Angiotensinogen; Angiotensinogen precursor; SERPINA 8… |
| Name | rotenone |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 16531806 | Lijnen P, Papparella I, Petrov V, Semplicini A, Fagard R: Angiotensin II-stimulated collagen production in cardiac fibroblasts is mediated by reactive species. J Hypertens. 2006 Apr;24(4):757-66. Rotenone, allopurinol, indomethacin, nordihydroguiaretic acid, ketoconazole and nitro- (inhibitors of mitochondrial NAD (P) H oxidase, xanthine oxidase, cyclooxygenase, lipoxygenase, cytochrome P450 oxygenase and synthase, respectively) did not affect the angiotensin II-induced collagen production. |
7(0,0,0,7) | Details |
| 15931622 | Ouslimani N, Peynet J, Bonnefont-Rousselot D, Therond P, Legrand A, Beaudeux JL: decreases intracellular production of reactive species in aortic endothelial cells. Metabolism. 2005 Jun;54(6):829-34. We investigated whether MET, at the pharmacological level of 10 -5 mol/L, was able to modulate intracellular production of reactive species (ROS) both in quiescent bovine aortic endothelial cells (BAECs) and in BAECs stimulated by a short incubation with high levels of (30 mmol/L, 2 hours) or angiotensin II (10 -7 mol/L, 1 hour). Experiments performed in the presence of the [NAD (P) H] oxidase inhibitor apocynin or the respiratory mitochondrial chain inhibitor rotenone indicated that MET exerted its effect partly through an inhibition of the formation of ROS produced mainly by NAD (P) H oxidase and also, to a lesser extent, by the respiratory mitochondrial chain. |
2(0,0,0,2) | Details |
| 18840762 | Eley HL, Russell ST, Tisdale MJ: Mechanism of attenuation of muscle protein degradation induced by tumor necrosis factor-alpha and angiotensin II by Am J Physiol Endocrinol Metab. 2008 Dec;295(6):E1417-26. Epub 2008 Oct 7. Formation of ROS was attenuated by rotenone, an inhibitor of the mitochondrial electron transport chain, nitro- methyl ester, an inhibitor of synthase, and SB 203580, a specific inhibitor of p38 mitogen-activated protein kinase (p38 MAPK), which also attenuated total protein degradation. |
2(0,0,0,2) | Details |
| 19781192 | Chen Y, Zhang AH, Huang SM, Ding GX, Zhang WZ, Bao HY, Wu HM, Chen RH: oxidase-derived reactive species involved in angiotensin II-induced monocyte chemoattractant protein-1 expression in mesangial cells]. Zhonghua Bing Li Xue Za Zhi. 2009 Jul;38(7):456-61. In contrast, inhibitors of other oxidant-producing enzymes, including the mitochondrial complex Iinhibitor rotenone, the xanthine oxidase inhibitor allopurinol, the cyclooxygenase inhibitor indomethacin, the lipoxygenase inhibitor nordihydroguiaretic acid, the cytochrome P450 oxygenase inhibitor ketoconazole and the synthase inhibitor G-nitro- methyl ester were without an effect. |
2(0,0,0,2) | Details |
| 12130563 | Hsieh TJ, Zhang SL, Filep JG, Tang SS, Ingelfinger JR, Chan JS: High glucose stimulates angiotensinogen gene expression via reactive species generation in rat kidney proximal tubular cells. Endocrinology. 2002 Aug;143(8):2975-85. These effects of high were blocked by antioxidants and tiron), inhibitors of mitochondrial electron transport chain complex I (rotenone) and II (thenoyltrifluoroacetone), an inhibitor of glycolysis-derived transport into mitochondria (alpha-cyano- an uncoupler of oxidative phosphorylation (carbonyl m-chlorophenylhydrazone), a manganese superoxide dismutase mimetic, catalase, and a specific inhibitor of p38 MAPK (SB 203580), but were not affected by an inhibitor of the - shuttle (aminooxyacetate acid). |
2(0,0,0,2) | Details |
| 9893134 | Heitzer T, Wenzel U, Hink U, Krollner D, Skatchkov M, Stahl RA, MacHarzina R, Brasen JH, Meinertz T, Munzel T: Increased NAD (P) H oxidase-mediated production in renovascular hypertension: evidence for an involvement of protein kinase C. Kidney Int. 1999 Jan;55(1):252-60. BACKGROUND: Angiotensin II infusion has been shown to cause hypertension and endothelial dysfunction and to increase (O-.2) production in vascular tissue, mainly via an activation of [NAD (P) H]-dependent oxidase, the most significant O-.2 source in endothelial and/or smooth muscle cells. Vascular O-.2 was normalized by the PKC inhibitor calphostin C, by the inhibitor of flavin-dependent oxidases, diphenylene iodonium, and recombinant -binding superoxide dismutase, whereas inhibitors of the xanthine oxidase synthase (NG-nitro- and mitochondrial NADH dehydrogenase (rotenone) were ineffective. |
1(0,0,0,1) | Details |
| 18801963 | Garciarena CD, Caldiz CI, Correa MV, Schinella GR, Mosca SM, Chiappe de Cingolani GE, Cingolani HE, Ennis IL: Na+/H+ exchanger-1 inhibitors decrease myocardial production via direct mitochondrial action. J Appl Physiol. 2008 Dec;105(6):1706-13. Epub 2008 Sep 18. Angiotensin II and endothelin-1 induced an oxidase (NOX)-dependent increase in anion (O (2)(-)) production detected by chemiluminescence. The mitochondria appeared to be the source of the NOX-dependent ROS released by the "ROS-induced ROS release mechanism" that was blunted by the mitochondrial ATP-sensitive potassium channel blockers 5-hydroxydecanoate and glibenclamide, inhibition of complex I of the electron transport chain with rotenone, and inhibition of the permeability transition pore (MPTP) by cyclosporin A. |
1(0,0,0,1) | Details |
| 10712386 | Pueyo ME, Gonzalez W, Nicoletti A, Savoie F, Arnal JF, Michel JB: Angiotensin II stimulates endothelial vascular cell adhesion molecule-1 via nuclear factor-kappaB activation induced by intracellular oxidative stress. Arterioscler Thromb Vasc Biol. 2000 Mar;20(3):645-51. In contrast, rotenone and antimycin, 2 inhibitors of the mitochondrial respiratory chain, inhibited the Ang II-induced IkappaB degradation, showing that generation of reactive species in the mitochondria is involved on Ang II action. |
88(1,1,1,8) | Details |
| 19028798 | Yamaguchi O, Kaneshiro T, Saitoh S, Ishibashi T, Maruyama Y, Takeishi Y: Regulation of coronary vascular tone via redox modulation in the alpha1-adrenergic-angiotensin-endothelin axis of the myocardium. Am J Physiol Heart Circ Physiol. 2009 Jan;296(1):H226-32. Epub 2008 Nov 21. These results suggest that alpha (1)-adrenergic stimulation in cardiac myocytes produces angiotensin I and H (2) O (2) and that angiotensin releases ET-1 through oxidase in coronary arterioles. Dihydroethidium (DHE) and dichlorodihydrofluorescein (DCF) intensities were increased by stimulation in isolated rat cardiac myocytes, which were enhanced by the mitochondrial electron transport chain complex I inhibitor rotenone (DHE: 20.4 +/- 1.2-fold and DCF: 25.2 +/- 0.9-fold, n = 8, P < 0.01, respectively) but not by the oxidase inhibitor apocynin. |
1(0,0,0,1) | Details |
| 15910763 | Grammatopoulos TN, Ahmadi F, Jones SM, Fariss MW, Weyhenmeyer JA, Zawada WM: Angiotensin II protects cultured midbrain dopaminergic neurons against rotenone-induced cell death. Brain Res. 2005 May 31;1045(1-2):64-71. Epub 2005 Apr 26. Ang II in the presence of the angiotensin type 1 receptor (AT1R) antagonist, losartan, was even more effective in protecting DA neurons showing a loss of only 13 +/- 4% at 20 nM rotenone. |
50(0,1,4,5) | Details |
| 7056751 | Reinhart PH, Taylor WM, Bygrave FL: Studies on alpha-adrenergic-induced respiration and glycogenolysis in perfused rat liver. J Biol Chem. 1982 Feb 25;257(4):1906-12. (1 milliunit/ml), and angiotensin II (6 x 10 (-9) M) had effects similar to in the perfused liver which also were prevented by the prior administration of antimycin A and rotenone. |
7(0,0,1,2) | Details |
| 9148750 | Rohacs T, Nagy G, Spat A: Cytoplasmic Ca2+ signalling and reduction of mitochondrial nucleotides in glomerulosa cells in response to K+, angiotensin II and Biochem J. 1997 Mar 15;322 ( Pt 3):785-92. applied after the addition of rotenone had no further effect, confirming that the redox signal was of mitochondrial origin. |
4(0,0,0,4) | Details |
| 20231142 | Villa-Abrille MC, Caldiz CI, Ennis IL, Nolly MB, Casarini MJ, Chiappe de Cingolani GE, Cingolani HE, Perez NG: The Anrep effect requires transactivation of the epidermal growth factor receptor. J Physiol. 2010 Mar 15. In this study we hypothesized that the SFR depends on epidermal growth factor receptor (EGFR) transactivation after the myocardial stretch-induced Ang II/ET release. EGF increased O2- production by 149+/-4% of control (n=9, P <0.05), effect canceled by inhibiting oxidase (apocynin, 110+/-6% n=7), mKATP channels (5-HD, 105+/-5%, n=8), respiratory chain (rotenone, 110+/-7%, n=7) or MPTP (Cyclosporine, 111+/-10%, n=6). |
2(0,0,0,2) | Details |
| 7460212 | Rounds S, McMurtry IF: Inhibitors of oxidative ATP production cause transient vasoconstriction and block subsequent pressor responses in rat lungs. Circ Res. 1981 Mar;48(3):393-400. The vascular reactivity of isolated, blood-perfused rat lungs was established by eliciting pressor responses to airway hypoxia and to intraarterial angiotensin II. Then, during normoxia, we added to perfusate one of five chemical inhibitors of oxidative ATP production: 10 mM azide, 1 mM 1 mM dinitrophenol, 5 or 10 microM antimycin A, or 0.5 microM rotenone. |
2(0,0,0,2) | Details |
| 18854758 | Nozoe M, Hirooka Y, Koga Y, Araki S, Konno S, Kishi T, Ide T, Sunagawa K: Mitochondria-derived reactive species mediate sympathoexcitation induced by angiotensin II in the rostral ventrolateral medulla. J Hypertens. 2008 Nov;26(11):2176-84. Overexpression of Mn-SOD and rotenone, a mitochondrial respiratory complex I inhibitor, suppressed AngII-induced ROS production. |
2(0,0,0,2) | Details |
| 19114648 | Chan SH, Wu KL, Chang AY, Tai MH, Chan JY: Oxidative impairment of mitochondrial electron transport chain complexes in rostral ventrolateral medulla contributes to neurogenic hypertension. Hypertension. 2009 Feb;53(2):217-27. Epub 2008 Dec 29. This mobile electron carrier also antagonized the elevated H (2) O (2) in RVLM and vasopressor responses to complex I (rotenone) or III (antimycin A) inhibitor in Wistar-Kyoto or prehypertensive rats. Intracerebroventricular infusion of angiotensin II promoted mitochondrial ETC dysfunctions in Wistar-Kyoto rats, and (10) or gene knockdown of the p22 (phox) subunit of oxidase antagonized the resultant elevation of H (2) O (2) in RVLM. |
1(0,0,0,1) | Details |