Published online before print August 19, 2002, doi: 10.1161/01.HYP.0000032100.23772.98
(Hypertension. 2002;40:511.)
© 2002 American Heart Association, Inc.
Scientific Contributions |
Role of p47phox in Vascular Oxidative Stress and Hypertension Caused by Angiotensin II
From the Division of Cardiology, Emory University School of Medicine and Atlanta Veterans Administration Hospital (U.L., H.C., S.D., L.M., J.H., H.J., D.G.H.), Atlanta, Ga; and Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health (S.M.H.), Bethesda, Md.
Correspondence to David G. Harrison, MD, Division of Cardiology, Emory University School of Medicine, 1639 Pierce Drive, 319 WMB, Atlanta, GA 30322. E-mail dharr02{at}emory.edu
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Hypertension caused by angiotensin II is dependent on vascular superoxide (O2·-) production. The nicotinamide adenine dinucleotide phosphate (NAD[P]H) oxidase is a major source of vascular O2·- and is activated by angiotensin II in vitro. However, its role in angiotensin II-induced hypertension in vivo is less clear. In the present studies, we used mice deficient in p47phox, a cytosolic subunit of the NADPH oxidase, to study the role of this enzyme system in vivo. In vivo, angiotensin II infusion (0.7 mg/kg per day for 7 days) increased systolic blood pressure from 105±2 to 151±6 mm Hg and increased vascular O2·- formation 2- to 3-fold in wild-type (WT) mice. In contrast, in p47phox-/- mice the hypertensive response to angiotensin II infusion (122±4 mm Hg; P<0.05) was markedly blunted, and there was no increase of vascular O2·- production. In situ staining for O2·- using dihydroethidium revealed a marked increase of O2·-production in both endothelial and vascular smooth muscle cells of angiotensin II-treated WT mice, but not in those of p47phox-/- mice. To directly examine the role of the NAD(P)H oxidase in endothelial production of O2·-, endothelial cells from WT and p47phox-/- mice were cultured. Western blotting confirmed the absence of p47phox in p47phox-/- mice. Angiotensin II increased O2·- production in endothelial cells from WT mice, but not in those from p47phox-/- mice, as determined by electron spin resonance spectroscopy. These results suggest a pivotal role of the NAD(P)H oxidase and its subunit p47phox in the vascular oxidant stress and the blood pressure response to angiotensin II in vivo.
Key Words: oxidative stress • endothelium • angiotensin II • hypertension, experimental
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Activation of the renin angiotensin system is critically involved in the pathogenesis of hypertension and atherosclerosis.1 The recently completed Heart Outcomes Prevention Evaluation (HOPE) trial demonstrated a remarkable decrease in cardiovascular morbidity and mortality by ACE inhibition in individuals at increased risk for cardiovascular events.2 A major mechanism whereby angiotensin II, the principal effector peptide of the renin-angiotensin system, may contribute to vascular pathology is stimulation of superoxide (O2·-) formation in vascular cells.3,4 We and others have shown that treatment with liposome-encapsulated superoxide dismutase (SOD) or the membrane-permeable SOD mimetic tempol markedly blunts the increase in blood pressure caused by angiotensin II administration, suggesting that stimulation of O2·- formation is critically involved in the blood pressure response to angiotensin II.5,6
One source of O2·- that is stimulated by angiotensin II in endothelial and vascular smooth muscle cells is the nicotinamide adenine dinucleotide phosphate (NAD[P]H) oxidase.3,7,8 Several recent in vitro studies have suggested an important role of the p47phox subunit of the NAD(P)H oxidase for angiotensin II stimulated O2·- production in vascular smooth muscle cells.8,9 It is not known, however, whether activation of the NAD(P)H oxidase and its subunit p47phox are critical for angiotensin II-stimulated O2·- production in endothelial cells. To address this issue, we studied mice lacking p47phox, a cytosolic subunit of the NAD(P)H oxidase,10 and examined responses to angiotensin II administered chronically in vivo. We also cultured endothelial cells from these mice and examined the effect of angiotensin II on O2·- production in vitro.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Animals Studied
Male C57BL/6 mice were obtained from Jackson Laboratories (25 to 35 g; Bar Harbor, Me) and were used at the age of 6 to 8 months. Male mice lacking p47phox10 were backcrossed at least x7 to the C57BL/6 background and were used at the age of 6 to 8 months. For implantation of osmotic minipumps, the mice were anesthetized with intraperitoneal Avertin 2.5% (0.3 mL per 25 g of body weight, IP). The intrascapular region was shaved, and an osmotic minipump (Alzet Model 2002; Alza Corp) that contained angiotensin II was inserted via a 1-cm incision to permit subcutaneous infusion of angiotensin II ([Val5]angiotensin II, infusion rate 0.7 mg/kg per day). Sham-operated animals underwent an identical surgical procedure, except that either no pump or an empty osmotic pump was implanted. On day 7 of angiotensin II infusion, the animals were killed by CO2 inhalation, and their aortas were harvested for study. The Emory University Institutional Animal Care and Use Committee approved all animal experiments.
Blood Pressure Measurement
Systolic blood pressures were measured by a computerized tail-cuff system (Visitech Systems).11 Before the osmotic pump was implanted, the mice were trained in the blood pressure device to accustom them to the procedure. On each day of blood pressure determination, 10 measurements were obtained and averaged for each mouse.
Measurements of Vascular Superoxide Production
Animals were euthanized by CO2 inhalation. The aortas were rapidly removed and placed into chilled modified Krebs/HEPES buffer (composition in mmol/L: NaCl 99.01, KCl 4.69, CaCl2 2.50, MgSO4 1.20, KH2PO4 1.03, NaHCO3 25.0, Na-HEPES 20.0, and glucose 5.6; pH 7.4), cleaned of excessive adventitial tissue, and cut into 4- to 5-mm ring segments with care taken not to injure the endothelium. Vascular O2·- production was determined using lucigenin-enhanced chemiluminescence as described before.12 This method has recently been validated for O2·- measurements in vascular tissue when low concentrations of lucigenin (5 µmol/L) are used.13,14
As a second approach to quantify vascular O2·- production, we employed dihydroethidium (HE) staining of intact vascular rings as described previously.15 Paired aortas from Angiotensin II-infused and sham animals were processed in parallel, and images were acquired with identical acquisition parameters. Reagents were purchased from Sigma-Aldrich.
Measurements of Superoxide Production in Cultured Endothelial Cells
Mouse aortic endothelial cells (MAECs) from wild-type and p47phox-/- mice were isolated using a matrigel culture as described previously and selected over vascular smooth muscle cells using heparin.16 Cells were maintained in DMEM (Gibco-BRL) containing 10% fetal calf serum (FCS, Hyclone Laboratories) supplemented with endothelial cell growth supplement (ECGS; 75 µg/mL; Sigma E-2759), heparin (10 U/mL), and antibiotics. Endothelial cells were used for studies at passage 3. On the day of confluence, the cell media was changed to DMEM with 5% serum overnight, and cells were studied the next day, one day post-confluency. Endothelial cell O2·- production was measured using electron-spin resonance spectroscopy (ESR) and the spin trap 1-hydroxy-3-carboxy-pyrrolidine (CP-H; Alexis Corporation). Cells were rinsed with ice-cold 50 mmol/L PBS buffer (pH 7.4) and removed from the plate by scrapping. After centrifugation at 800g (7 minutes), the cells were resuspended in 400 µL PBS buffer and kept on ice. To inhibit iron-catalyzed oxidation of the spin trap, DTPA (0.2 mmol/L) was added to all samples. ESR measurements were performed in 50-µL glass capillaries (Corning). The ESR spectra were recorded using a Bruker EMX spectrometer (Bruker Corporation) and a super-high Q microwave cavity. O2·- formation was determined by following the oxidation of CP-H to paramagnetic 3-carboxy-proxyl (CP·).17,18 The ESR instrumental settings were as follows: field sweep, 50 G; microwave frequency, 9.78 GHz; microwave power, 20 mW; modulation amplitude, 2 G; conversion time, 656 ms; time constant, 656 ms; 512 points resolution and receiver gain, 1x105 (74 dB). Time scans were recorded using 1312 ms conversion time, 5248 ms time constant, and monitoring the ESR amplitude of low-field component of ESR spectrum of carboxy-proxyl nitroxide for 300 s.
Immunoblot Analysis of p47phox and Angiotensin II Type 1-Receptor Expression in Endothelial Cells
Protein samples were prepared from mouse aortic endothelial cells and lysed directly in SDS sample buffer. Protein from endothelial cell lysates (20 µg) was separated by SDS-PAGE, transferred to membranes, and probed with anti-p47phox antibody (BD Transduction Laboratories) or angiotensin II type 1 (AT1)-receptor antibody (Santa Cruz Biotechnology). For the p47phox immunoblot analysis, mouse macrophage lysates (10 µg) were loaded as positive controls. Protein was visualized by chemiluminescence.
Data Analysis
All data are expressed as mean±SEM. Comparisons between groups of animals or treatments were made by one-way ANOVA, followed by Student-Newman-Keuls test. Values of P<0.05 were considered statistically significant.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Effects of Angiotensin II Treatment on Vascular Superoxide Production in Wild-Type (C57/BL6) and p47phox-/- Mice
Angiotensin II infusion caused a 2- to 3-fold increase in vascular O2·- production in wild-type (C57/BL6) mice (Figure 1a). In contrast, in p47phox-/- mice, no increase in vascular O2·- formation was observed after treatment with angiotensin II (Figure 1a). To estimate O2·- production in mouse aortas in situ, we used HE staining. Conversion of HE by O2·- to ethidium results in nuclear fluorescence. Aortas from angiotensin II-treated wild-type mice consistently showed a markedly increased fluorescence, both in the endothelium and in vascular smooth muscle, indicating increased O2·- production (Figure 1b). In p47phox-/- mice, however, no increase in HE-detectable O2·- production was observed after angiotensin II infusion (Figure 1b).
|
Effect of Angiotensin II Treatment on Blood Pressure in Wild-Type and p47phox-/- Mice
In wild-type mice, angiotensin II infusion caused an increase in blood pressure from 105±2 to 151±6 mm Hg (Figure 2). Importantly, in p47phox-/- mice, the blood pressure response to angiotensin II was markedly blunted (Figure 2).
|
Effect of Angiotensin II on Superoxide Production in Cultured Endothelial Cells from Wild-Type and p47phox-/- Mice
To study the role of p47phox in angiotensin II-induced O2·- formation in endothelial cells independent of changes in blood pressure we measured O2·- formation in cultured endothelial cells from wild-type and p47phox-/- mice. Whereas in wild-type endothelial cells, angiotensin II administration (10-6 mol/L) caused a substantial increase in CP-H oxidation, there was no change in CP-H oxidation in p47phox-deficient endothelial cells in response to angiotensin II (Figures 3a and 3b). The increase of CP-H oxidation caused by angiotensin II in wild-type endothelial cells was completely inhibited by superoxide dismutase (50 U PEG-SOD), indicating that CP-H oxidation was caused by O2·- (Figure 3a).
|
Immunoblot Analysis of p47phox and AT1-Receptor Expression in Endothelial Cells
The p47phox subunit of the NAD(P)H oxidase was expressed in aortic endothelial cells from wild-type mice but not in endothelial cells cultured from p47phox-deficient mice (Figure 3c). The expression of the AT1 receptor was similar in p47phox-deficient and wild-type endothelial cells (Figure 3d).
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Our present results demonstrate a critical role of the NAD(P)H oxidase and its subunit p47phox for the vascular oxidant stress response to angiotensin II. The increase in vascular O2·- production in response to angiotensin II administration was diminished in p47phox-/- mice and the amount of hypertension caused by angiotensin II was reduced in these animals compared with wild-type mice. Angiotensin II stimulated O2·- production in cultured aortic endothelial cells from wild-type mice but not in p47phox-deficient endothelial cells.
We have previously shown that angiotensin II administration in rats causes a substantial increase in vascular O2·- formation and impairs endothelium-dependent vasodilation.4 Treatment with liposome-encapsulated superoxide dismutase (SOD) or the membrane-permeable SOD mimetic tempol blunts the increase in blood pressure caused by angiotensin II and preserves the bioavailability of nitric oxide, suggesting that the increase in vascular O2·- formation is critical for the blood response to the octapeptide.5,6 An important source of O2·- in endothelial and vascular smooth muscle cells is the NAD(P)H oxidase, 3,19 which is stimulated by angiotensin II in both cell types.3,7–9 In addition, increased vascular NAD(P)H oxidase activity and increased expression of its subunit p22phox was observed in angiotensin II-treated rats in vivo,4,20 raising the question whether activation of this enzyme complex is critical for the oxidant stress and blood pressure response to angiotensin II. In the present studies, we used mice deficient in p47phox,10 a cytosolic subunit of the NAD(P)H oxidase, to address this question. Whereas angiotensin II administration caused a 2- to 3-fold increase of vascular O2·- production in wild-type mice, no such increase was observed in p47phox-deficient mice after angiotensin II treatment. Importantly, the blood pressure response to angiotensin II was markedly blunted in mice lacking p47phox compared with wild-type mice, suggesting a pivotal role of NAD(P)H oxidase activation for the blood pressure increase caused by angiotensin II.
In addition to smooth muscle cells, a major source of vascular O2·- stimulated by angiotensin II in vivo appears to be the endothelium. In wild-type, but not in p47phox-deficient mice, there was a marked increase of endothelial O2·- production evoked by angiotensin II as detected by HE fluorescent staining. Lavigne et al have recently demonstrated the requirement of p47phox for angiotensin II-stimulated O2·- production in vascular smooth muscle cells in vitro.8 In the present study, we therefore analyzed the role of p47phox in angiotensin II-induced oxidant stress in endothelial cells. In cultured endothelial cells from wild-type mice, but not in p47phox-deficient cells, there was a marked increase of O2·- formation after exposure to angiotensin II as revealed by ESR spectroscopy, suggesting that activation of the NAD(P)H oxidase within the endothelium is dependent on p47phox. One possible explanation for there being less O2·- formation in response to angiotensin II in p47phox-deficient endothelial cells could be a reduced AT1-receptor gene expression. Our Western blot analysis, however, showed similar expression of the AT1 receptor in p47phox-deficient and wild-type endothelial cells.
Basal O2·- production was similar in endothelial cells from wild-type and p47phox-deficient mice, suggesting that p47phox is not essential for basal O2·- formation in endothelial cells. There are other sources of O2·- (ie, xanthine oxidase, cytochrome p450, mitochondria), which could also account for basal O2·- formation in p47phox-deficient cells. Our results are compatible with the recent findings of Li et al21 in cultured coronary microvascular endothelial cells from p47phox-deficient mice, who found no reduction in basal O2·- production, but a reduced response to TNF-
and phorbol ester in p47phox-deficient microvascular endothelial cells.21
In the present study, we observed expression of p47phox in aortic endothelial cells from wild-type, but not from p47phox-deficient mice. The expression of the NAD(P)H oxidase subunit p47phox has been demonstrated in other endothelial cell lines, ie, human umbilical vein endothelial cells and murine microvascular endothelial cells.21,22 In neutrophils the importance of p47phox for activation of the NAD(P)H oxidase is well documented because its phosphorylation appears to be the limiting step required for assembly of the active enzyme complex.23 Furthermore, mutations of p47phox are a cause of chronic granulomatous disease, an immune deficiency resulting from impaired phagocyte activity.23 The results of the present studies suggest that p47phox is equally vital to the activation of the NAD(P)H oxidase by angiotensin II within the endothelium.
Perspectives
In summary, the present study indicates that the NAD(P)H oxidase and its cytosolic subunit p47phox play a pivotal role in mediating the hypertension caused by angiotensin II. Our results are in keeping with a recent study by Rey et al who demonstrated that treatment with a chimeric peptide designed to inhibit the association of p47phox with the NAD(P)H oxidase membrane components diminished the blood pressure response to angiotensin II.24 Our experiments also show that p47phox and the NAD(P)H oxidase are essential for angiotensin II-stimulated O2· production in cultured aortic endothelial cells. Increased endothelial O2·- production in response to angiotensin II may also be important for the proinflammatory and proatherogenic effects of the octapeptide. Stokes et al25 have recently demonstrated that p47phox deficiency diminished the hypercholesterolemia-induced leukocyte-endothelial cell adhesion, and we have previously shown that activation of the vascular NAD(P)H oxidase in hypercholesterolemia is dependent on angiotensin II.26 Furthermore, when crossed with p47phox-/- mice, apolipoprotein E (Apo[e])-deficient mice have a rather marked reduction in atherosclerosis in the descending aorta compared with mice lacking only Apo(e).27 Given these now very clear crucial roles in vascular disease, the NAD(P)H oxidase and p47phox represent important targets for therapeutic intervention, and their specific inhibitors would very likely be useful in treatment of common disorders such as hypertension and atherosclerosis.
|
Acknowledgments |
|---|
We gratefully acknowledge excellent technical support by Graciela Gamez. This work was supported by National Institutes of Health (NIH) grants HL390006 (D.G.H.) and HL59248 (D.G.H.), NIH Program Project Grant HL58000 (D.G.H.), and a Department of Veterans Affairs merit grant (D.G.H.). U.L. was supported by a grant from the German Cardiac Society and the Feodor Lynen Grant of the Alexander von Humboldt Foundation.
Received April 29, 2002; first decision May 9, 2002; accepted July 15, 2002.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Nickenig G, Harrison DG. The AT(1)-type angiotensin receptor in oxidative stress and atherogenesis. I. Oxidative stress and atherogenesis. Circulation. 2002; 105: 393–396.
2. Yusuf S, Sleight P, Pogue J, Bosch J, Davies R, Dagenais G. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N Engl J Med. 2000; 342: 145–153.
3. Griendling KK, Minieri CA, Ollerenshaw JD, Alexander RW. Angiotensin II stimulates NADH and NAD(P)H oxidase activity in cultured vascular smooth muscle cells. Circ Res. 1994; 74: 1141–1148.
4. Rajagopalan S, Kurz S, Munzel T, Tarpey M, Freeman BA, Griendling KK, Harrison DG. Angiotensin II-mediated hypertension in the rat increases vascular superoxide production via membrane NADH/NAD(P)H oxidase activation. Contribution to alterations of vasomotor tone. J Clin Invest. 1996; 97: 1916–1923.[Medline] [Order article via Infotrieve]
5. Laursen JB, Rajagopalan S, Galis Z, Tarpey M, Freeman BA, Harrison DG. Role of superoxide in angiotensin II-induced but not catecholamine-induced hypertension. Circulation. 1997; 95: 588–593.
6. Nishiyama A, Fukui T, Fujisawa Y, Rahman M, Tian RX, Kimura S, Abe Y. Systemic and regional hemodynamic responses to tempol in angiotensin II-infused hypertensive rats. Hypertension. 2001; 37: 77–83.
7. Zhang H, Schmeisser A, Garlichs CD, Plotze K, Damme U, Mugge A, Daniel WG. Angiotensin II-induced superoxide anion generation in human vascular endothelial cells: role of membrane-bound NADH-/NADPH-oxidases. Cardiovasc Res. 1999; 44: 215–222.
8. Lavigne MC, Malech HL, Holland SM, Leto TL. Genetic demonstration of p47phox-dependent superoxide anion production in murine vascular smooth muscle cells. Circulation. 2001; 104: 79–84.
9. Schieffer B, Luchtefeld M, Braun S, Hilfiker A, Hilfiker-Kleiner D, Drexler H. Role of NAD(P)H oxidase in angiotensin II-induced JAK/STAT signaling and cytokine induction. Circ Res. 2000; 87: 1195–1201.
10. Jackson SH, Gallin JI, Holland SM. The p47phox mouse knock-out model of chronic granulomatous disease. J Exp Med. 1995; 182: 751–758.
11. Krege JH, Hodgin JB, Hagaman JR, Smithies O. A noninvasive computerized tail-cuff system for measuring blood pressure in mice. Hypertension. 1995; 25: 1111–1115.
12. Laursen JB, Somers M, Kurz S, McCann L, Warnholtz A, Freeman BA, Tarpey M, Fukai T, Harrison DG. Endothelial regulation of vasomotion in apoE-deficient mice: implications for interactions between peroxynitrite and tetrahydrobiopterin. Circulation. 2001; 103: 1282–1288.
13. Skatchkov MP, Sperling D, Hink U, Mulsch A, Harrison DG, Sindermann I, Meinertz T, Munzel T. Validation of lucigenin as a chemiluminescent probe to monitor vascular superoxide as well as basal vascular nitric oxide production. Biochem Biophys Res Commun. 1999; 254: 319–324.[CrossRef][Medline] [Order article via Infotrieve]
14. Li Y, Zhu H, Kuppusamy P, Roubaud V, Zweier JL, Trush MA. Validation of lucigenin (bis-N-methylacridinium) as a chemilumigenic probe for detecting superoxide anion radical production by enzymatic and cellular systems. J Biol Chem. 1998; 273: 2015–2023.
15. Somers MJ, Mavromatis K, Galis ZS, Harrison DG. Vascular superoxide production and vasomotor function in hypertension induced by deoxycorticosterone acetate-salt. Circulation. 2000; 101: 1722–1728.
16. Suh SH, Vennekens R, Manolopoulos VG, Freichel M, Schweig U, Prenen J, Flockerzi V, Droogmans G, Nilius B. Characterization of explanted endothelial cells from mouse aorta: electrophysiology and Ca2+ signaling. Pflugers Arch. 1999; 438: 612–620.[CrossRef][Medline] [Order article via Infotrieve]
17. Dikalov S, Skatchkov M, Bassenge E. Spin trapping of superoxide radicals and peroxynitrite by 1-hydroxy-3-carboxy-pyrrolidine and 1-hydroxy-2,2,6,6-tetramethyl-4-oxo-piperidine and the stability of corresponding nitroxyl radicals towards biological reductants. Biochem Biophys Res Commun. 1997; 231: 701–704.[CrossRef][Medline] [Order article via Infotrieve]
18. Dikalov S, Fink B, Skatchkov M, Bassenge E. Comparison of glyceryl trinitrate-induced with pentaerythrityl tetranitrate-induced in vivo formation of superoxide radicals: effect of vitamin C. Free Radic Biol Med. 1999; 27: 170–176.[CrossRef][Medline] [Order article via Infotrieve]
19. Somers MJ, Burchfield JS, Harrison DG. Evidence for a NADH/NAD(P)H oxidase in human umbilical vein endothelial cells using electron spin resonance. Antioxid Redox Signal. 2000; 2: 779–787.[Medline] [Order article via Infotrieve]
20. Fukui T, Ishizaka N, Rajagopalan S, Laursen JB, Capers Qt, Taylor WR, Harrison DG, de Leon H, Wilcox JN, Griendling KK. p22phox mRNA expression and NAD(P)H oxidase activity are increased in aortas from hypertensive rats. Circ Res. 1997; 80: 45–51.
21. Li JM, Mullen AM, Yun S, Wientjes F, Brouns GY, Thrasher AJ, Shah AM. Essential role of the NAD(P)H oxidase subunit p47(phox) in endothelial cell superoxide production in response to phorbol ester and tumor necrosis factor-alpha. Circ Res. 2002; 90: 143–150.
22. Jones SA, O’Donnell VB, Wood JD, Broughton JP, Hughes EJ, Jones OT. Expression of phagocyte NAD(P)H oxidase components in human endothelial cells. Am J Physiol. 1996; 271: H1626–H1634.[Medline] [Order article via Infotrieve]
23. Babior BM. NADPH oxidase: an update. Blood. 1999; 93: 1464–1476.
24. Rey FE, Cifuentes ME, Kiarash A, Quinn MT, Pagano PJ. Novel competitive inhibitor of NAD(P)H oxidase assembly attenuates vascular O(2)(-) and systolic blood pressure in mice. Circ Res. 2001; 89: 408–414.
25. Stokes KY, Clanton EC, Russell JM, Ross CR, Granger DN. NAD(P)H oxidase-derived superoxide mediates hypercholesterolemia-induced leukocyte-endothelial cell adhesion. Circ Res. 2001; 88: 499–505.
26. Warnholtz A, Nickenig G, Schulz E, Macharzina R, Brasen JH, Skatchkov M, Heitzer T, Stasch JP, Griendling KK, Harrison DG, Bohm M, Meinertz T, Munzel T. Increased NADH-oxidase-mediated superoxide production in the early stages of atherosclerosis: evidence for involvement of the renin-angiotensin system. Circulation. 1999; 99: 2027–2033.
27. Barry-Lane PA, Patterson C, van der Merwe M, Hu Z, Holland SM, Yeh ET, Runge MS. p47phox is required for atherosclerotic lesion progression in ApoE(-/-) mice. J Clin Invest. 2001; 108: 1513–1522.[CrossRef][Medline] [Order article via Infotrieve]
This article has been cited by other articles:
 |
|
 |
|
  C. Gimpel and F. Schaefer Williams-Beuren syndrome--stretching to learn big lessons from small patients Nephrol. Dial. Transplant., November 24, 2009; (2009) gfp614v1. [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Wang and Z. Sun Klotho Gene Delivery Prevents the Progression of Spontaneous Hypertension and Renal Damage Hypertension, October 1, 2009; 54(4): 810 - 817. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Maloney, I. R. Sweet, D. M. Hockenbery, M. Pham, N. O. Rizzo, S. Tateya, P. Handa, M. W. Schwartz, and F. Kim Activation of NF-{kappa}B by Palmitate in Endothelial Cells: A Key Role for NADPH Oxidase-Derived Superoxide in Response to TLR4 Activation Arterioscler Thromb Vasc Biol, September 1, 2009; 29(9): 1370 - 1375. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. D. Widder, D. Fraccarollo, P. Galuppo, J. M. Hansen, D. P. Jones, G. Ertl, and J. Bauersachs Attenuation of Angiotensin II-Induced Vascular Dysfunction and Hypertension by Overexpression of Thioredoxin 2 Hypertension, August 1, 2009; 54(2): 338 - 344. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Walter, N. Etienne-Selloum, D. Brasse, R. Schleiffer, V. Bekaert, P. M. Vanhoutte, A. Beretz, and V. B. Schini-Kerth Red Wine Polyphenols Prevent Acceleration of Neovascularization by Angiotensin II in the Ischemic Rat Hindlimb J. Pharmacol. Exp. Ther., May 1, 2009; 329(2): 699 - 707. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. J. Ryan Young Investigator Award Lecture of the APS Water and Electrolyte Homeostasis Section, 2008: The pathophysiology of hypertension in systemic lupus erythematosus Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2009; 296(4): R1258 - R1267. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. G. Mayhan, D. M. Arrick, G. M. Sharpe, and H. Sun Nitric oxide synthase-dependent responses of the basilar artery during acute infusion of nicotine Nicotine Tob Res, March 1, 2009; 11(3): 270 - 277. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. A. Miller, G. R. Drummond, T. M. De Silva, A. E. Mast, H. Hickey, J. P. Williams, B. R. S. Broughton, and C. G. Sobey NADPH oxidase activity is higher in cerebral versus systemic arteries of four animal species: role of Nox2 Am J Physiol Heart Circ Physiol, January 1, 2009; 296(1): H220 - H225. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P.-S. Tsou, V. Addanki, and H.-L. Fung Dissociation between Superoxide Accumulation and Nitroglycerin-Induced Tolerance J. Pharmacol. Exp. Ther., October 1, 2008; 327(1): 97 - 104. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 X. W. Cheng, T. Murohara, M. Kuzuya, H. Izawa, T. Sasaki, K. Obata, K. Nagata, T. Nishizawa, M. Kobayashi, T. Yamada, et al. Superoxide-Dependent Cathepsin Activation Is Associated with Hypertensive Myocardial Remodeling and Represents a Target for Angiotensin II Type 1 Receptor Blocker Treatment Am. J. Pathol., August 1, 2008; 173(2): 358 - 369. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. M. Diaz Encarnacion, G. M. Warner, C. E. Gray, J. Cheng, H. K. H. Keryakos, K. A. Nath, and J. P. Grande Signaling pathways modulated by fish oil in salt-sensitive hypertension Am J Physiol Renal Physiol, June 1, 2008; 294(6): F1323 - F1335. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Jin, Y. Zhang, F. Yi, and P.-L. Li Critical Role of Lipid Raft Redox Signaling Platforms in Endostatin-Induced Coronary Endothelial Dysfunction Arterioscler Thromb Vasc Biol, March 1, 2008; 28(3): 485 - 490. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Uemura, H. Ishiguro, Y. Ishiguro, K. Hoshino, S. Takahashi, and Y. Kubota Angiotensin II Induces Oxidative Stress in Prostate Cancer Mol. Cancer Res., February 1, 2008; 6(2): 250 - 258. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. M. Paravicini and R. M. Touyz NADPH Oxidases, Reactive Oxygen Species, and Hypertension: Clinical implications and therapeutic possibilities Diabetes Care, February 1, 2008; 31(Supplement_2): S170 - S180. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Choi, T. L. Leto, L. Hunyady, K. J. Catt, Y. S. Bae, and S. G. Rhee Mechanism of Angiotensin II-induced Superoxide Production in Cells Reconstituted with Angiotensin Type 1 Receptor and the Components of NADPH Oxidase J. Biol. Chem., January 4, 2008; 283(1): 255 - 267. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Adachi, M. Yamamoto, and M. Suematsu Targeting NAD(P)H Oxidase: Ets-1 Regulates p47phox Circ. Res., November 9, 2007; 101(10): 962 - 964. [Full Text] [PDF]
|
|
|
|
|
|
W. Ni, Y. Zhan, H. He, E. Maynard, J. A. Balschi, and P. Oettgen Ets-1 Is a Critical Transcriptional Regulator of Reactive Oxygen Species and p47phox Gene Expression in Response to Angiotensin II Circ. Res., November 9, 2007; 101(10): 985 - 994. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G.-X. Zhang, X.-M. Lu, S. Kimura, and A. Nishiyama Role of mitochondria in angiotensin II-induced reactive oxygen species and mitogen-activated protein kinase activation Cardiovasc Res, November 1, 2007; 76(2): 204 - 212. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. J. Guzik, N. E. Hoch, K. A. Brown, L. A. McCann, A. Rahman, S. Dikalov, J. Goronzy, C. Weyand, and D. G. Harrison Role of the T cell in the genesis of angiotensin II induced hypertension and vascular dysfunction J. Exp. Med., October 1, 2007; 204(10): 2449 - 2460. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. A. Sorrentino, F. H. Bahlmann, C. Besler, M. Muller, S. Schulz, N. Kirchhoff, C. Doerries, T. Horvath, A. Limbourg, F. Limbourg, et al. Oxidant Stress Impairs In Vivo Reendothelialization Capacity of Endothelial Progenitor Cells From Patients With Type 2 Diabetes Mellitus: Restoration by the Peroxisome Proliferator-Activated Receptor-{gamma} Agonist Rosiglitazone Circulation, July 10, 2007; 116(2): 163 - 173. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Liu, J. L. Garvin, Y. Ren, P. J. Pagano, and O. A. Carretero Depolarization of the macula densa induces superoxide production via NAD(P)H oxidase Am J Physiol Renal Physiol, June 1, 2007; 292(6): F1867 - F1872. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. K. Bendall, R. Rinze, D. Adlam, A. L. Tatham, J. de Bono, and K. M. Channon Endothelial Nox2 Overexpression Potentiates Vascular Oxidative Stress and Hemodynamic Response to Angiotensin II: Studies in Endothelial-Targeted Nox2 Transgenic Mice Circ. Res., April 13, 2007; 100(7): 1016 - 1025. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
U. Landmesser, S. Spiekermann, C. Preuss, S. Sorrentino, D. Fischer, C. Manes, M. Mueller, and H. Drexler Angiotensin II Induces Endothelial Xanthine Oxidase Activation: Role for Endothelial Dysfunction in Patients With Coronary Disease Arterioscler Thromb Vasc Biol, April 1, 2007; 27(4): 943 - 948. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. D. Widder, T. J. Guzik, C. F.H. Mueller, R. E. Clempus, H. H.H.W. Schmidt, S. I. Dikalov, K. K. Griendling, D. P. Jones, and D. G. Harrison Role of the Multidrug Resistance Protein-1 in Hypertension and Vascular Dysfunction Caused by Angiotensin II Arterioscler Thromb Vasc Biol, April 1, 2007; 27(4): 762 - 768. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Doerries, K. Grote, D. Hilfiker-Kleiner, M. Luchtefeld, A. Schaefer, S. M. Holland, S. Sorrentino, C. Manes, B. Schieffer, H. Drexler, et al. Critical Role of the NAD(P)H Oxidase Subunit p47phox for Left Ventricular Remodeling/Dysfunction and Survival After Myocardial Infarction Circ. Res., March 30, 2007; 100(6): 894 - 903. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Patwari and R. T. Lee Thioredoxins, Mitochondria, and Hypertension Am. J. Pathol., March 1, 2007; 170(3): 805 - 808. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. Armando, X. Wang, V. A. M. Villar, J. E. Jones, L. D. Asico, C. Escano, and P. A. Jose Reactive Oxygen Species-Dependent Hypertension in Dopamine D2 Receptor-Deficient Mice Hypertension, March 1, 2007; 49(3): 672 - 678. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Szasz, K. Thakali, G. D. Fink, and S. W. Watts A Comparison of Arteries and Veins in Oxidative Stress: Producers, Destroyers, Function, and Disease Experimental Biology and Medicine, January 1, 2007; 232(1): 27 - 37. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Bedard and K.-H. Krause The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology Physiol Rev, January 1, 2007; 87(1): 245 - 313. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Zhang, F. Zhang, R. Muh, F. Yi, K. Chalupsky, H. Cai, and P.-L. Li Autocrine/paracrine pattern of superoxide production through NAD(P)H oxidase in coronary arterial myocytes Am J Physiol Heart Circ Physiol, January 1, 2007; 292(1): H483 - H495. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Wang, A. F. Chen, and D. H. Wang Enhanced oxidative stress in kidneys of salt-sensitive hypertension: role of sensory nerves Am J Physiol Heart Circ Physiol, December 1, 2006; 291(6): H3136 - H3143. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Wei, J. R. Sowers, R. Nistala, H. Gong, G. M.-E. Uptergrove, S. E. Clark, E. M. Morris, N. Szary, C. Manrique, and C. S. Stump Angiotensin II-induced NADPH Oxidase Activation Impairs Insulin Signaling in Skeletal Muscle Cells J. Biol. Chem., November 17, 2006; 281(46): 35137 - 35146. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Feletou and P. M. Vanhoutte Endothelial dysfunction: a multifaceted disorder (The Wiggers Award Lecture) Am J Physiol Heart Circ Physiol, September 1, 2006; 291(3): H985 - H1002. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Sarr, M. Chataigneau, S. Martins, C. Schott, J. El Bedoui, M.-H. Oak, B. Muller, T. Chataigneau, and V. B. Schini-Kerth Red wine polyphenols prevent angiotensin II-induced hypertension and endothelial dysfunction in rats: Role of NADPH oxidase Cardiovasc Res, September 1, 2006; 71(4): 794 - 802. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Grote, M. Ortmann, G. Salguero, C. Doerries, U. Landmesser, M. Luchtefeld, R. P. Brandes, W. Gwinner, T. Tschernig, E.-G. Brabant, et al. Critical role for p47phox in renin-angiotensin system activation and blood pressure regulation Cardiovasc Res, August 1, 2006; 71(3): 596 - 605. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Thomas, D. Gavrila, M. L. McCormick, F. J. Miller Jr, A. Daugherty, L. A. Cassis, K. C. Dellsperger, and N. L. Weintraub Deletion of p47phox Attenuates Angiotensin II-Induced Abdominal Aortic Aneurysm Formation in Apolipoprotein E-Deficient Mice Circulation, August 1, 2006; 114(5): 404 - 413. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. M. Paravicini and R. M. Touyz Redox signaling in hypertension Cardiovasc Res, July 15, 2006; 71(2): 247 - 258. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Nagata, M. Takahashi, K. Sawai, T. Tagami, T. Usui, A. Shimatsu, Y. Hirata, and M. Naruse Molecular Mechanism of the Inhibitory Effect of Aldosterone on Endothelial NO Synthase Activity Hypertension, July 1, 2006; 48(1): 165 - 171. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Miriyala, M. C. Gongora Nieto, C. Mingone, D. Smith, S. Dikalov, D. G. Harrison, and H. Jo Bone Morphogenic Protein-4 Induces Hypertension in Mice: Role of Noggin, Vascular NADPH Oxidases, and Impaired Vasorelaxation Circulation, June 20, 2006; 113(24): 2818 - 2825. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Hunyady and K. J. Catt Pleiotropic AT1 Receptor Signaling Pathways Mediating Physiological and Pathogenic Actions of Angiotensin II Mol. Endocrinol., May 1, 2006; 20(5): 953 - 970. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Menshikov, O. Plekhanova, H. Cai, K. Chalupsky, Y. Parfyonova, P. Bashtrikov, V. Tkachuk, and B. C. Berk Urokinase Plasminogen Activator Stimulates Vascular Smooth Muscle Cell Proliferation Via Redox-Dependent Pathways Arterioscler Thromb Vasc Biol, April 1, 2006; 26(4): 801 - 807. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. E. Taylor, P. Glocka, M. Liang, and A. W. Cowley Jr NADPH Oxidase in the Renal Medulla Causes Oxidative Stress and Contributes to Salt-Sensitive Hypertension in Dahl S Rats Hypertension, April 1, 2006; 47(4): 692 - 698. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Modlinger, T. Chabrashvili, P. S. Gill, M. Mendonca, D. G. Harrison, K. K. Griendling, M. Li, J. Raggio, A. Wellstein, Y. Chen, et al. RNA Silencing In Vivo Reveals Role of p22phox in Rat Angiotensin Slow Pressor Response Hypertension, February 1, 2006; 47(2): 238 - 244. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Wang, J. Zhang, G. Spinetti, L.-Q. Jiang, R. Monticone, D. Zhao, L. Cheng, M. Krawczyk, M. Talan, G. Pintus, et al. Angiotensin II Activates Matrix Metalloproteinase Type II and Mimics Age-Associated Carotid Arterial Remodeling in Young Rats Am. J. Pathol., November 1, 2005; 167(5): 1429 - 1442. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. P. Didion, D. A. Kinzenbaw, and F. M. Faraci Critical Role for CuZn-Superoxide Dismutase in Preventing Angiotensin II-Induced Endothelial Dysfunction Hypertension, November 1, 2005; 46(5): 1147 - 1153. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Matsuno, H. Yamada, K. Iwata, D. Jin, M. Katsuyama, M. Matsuki, S. Takai, K. Yamanishi, M. Miyazaki, H. Matsubara, et al. Nox1 Is Involved in Angiotensin II-Mediated Hypertension: A Study in Nox1-Deficient Mice Circulation, October 25, 2005; 112(17): 2677 - 2685. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Dikalova, R. Clempus, B. Lassegue, G. Cheng, J. McCoy, S. Dikalov, A. S. Martin, A. Lyle, D. S. Weber, D. Weiss, et al. Nox1 Overexpression Potentiates Angiotensin II-Induced Hypertension and Vascular Smooth Muscle Hypertrophy in Transgenic Mice Circulation, October 25, 2005; 112(17): 2668 - 2676. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. S. Wilcox Oxidative stress and nitric oxide deficiency in the kidney: a critical link to hypertension? Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2005; 289(4): R913 - R935. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Castier, R. P. Brandes, G. Leseche, A. Tedgui, and S. Lehoux p47phox-Dependent NADPH Oxidase Regulates Flow-Induced Vascular Remodeling Circ. Res., September 16, 2005; 97(6): 533 - 540. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. L. Park, R. D. Loberg, D. Duquaine, H. Zhang, B. K. Deo, N. Ardanaz, J. Coyle, K. B. Atkins, M. Schin, M. J. Charron, et al. GLUT4 Facilitative Glucose Transporter Specifically and Differentially Contributes to Agonist-Induced Vascular Reactivity in Mouse Aorta Arterioscler Thromb Vasc Biol, August 1, 2005; 25(8): 1596 - 1602. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. E. Ullian, A. K. Gelasco, W. R. Fitzgibbon, C. N. Beck, and T. A. Morinelli N-Acetylcysteine Decreases Angiotensin II Receptor Binding in Vascular Smooth Muscle Cells J. Am. Soc. Nephrol., August 1, 2005; 16(8): 2346 - 2353. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Matsui, S. Xu, K. A. Maitland, A. Hayes, J. A. Leopold, D. E. Handy, J. Loscalzo, and R. A. Cohen Glucose-6 Phosphate Dehydrogenase Deficiency Decreases the Vascular Response to Angiotensin II Circulation, July 12, 2005; 112(2): 257 - 263. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Chalupsky and H. Cai Endothelial dihydrofolate reductase: Critical for nitric oxide bioavailability and role in angiotensin II uncoupling of endothelial nitric oxide synthase PNAS, June 21, 2005; 102(25): 9056 - 9061. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Wesseling, D. A. Ishola Jr., J. A. Joles, H. A. Bluyssen, H. A. Koomans, and B. Braam Resistance to oxidative stress by chronic infusion of angiotensin II in mouse kidney is not mediated by the AT2 receptor Am J Physiol Renal Physiol, June 1, 2005; 288(6): F1191 - F1200. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Akishita, K. Nagai, H. Xi, W. Yu, N. Sudoh, T. Watanabe, M. Ohara-Imaizumi, S. Nagamatsu, K. Kozaki, M. Horiuchi, et al. Renin-Angiotensin System Modulates Oxidative Stress-Induced Endothelial Cell Apoptosis in Rats Hypertension, June 1, 2005; 45(6): 1188 - 1193. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. R. Madamanchi, S.-K. Moon, Z. S. Hakim, S. Clark, A. Mehrizi, C. Patterson, and M. S. Runge Differential Activation of Mitogenic Signaling Pathways in Aortic Smooth Muscle Cells Deficient in Superoxide Dismutase Isoforms Arterioscler Thromb Vasc Biol, May 1, 2005; 25(5): 950 - 956. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Kimura, G.-X. Zhang, A. Nishiyama, T. Shokoji, L. Yao, Y.-Y. Fan, M. Rahman, T. Suzuki, H. Maeta, and Y. Abe Role of NAD(P)H Oxidase- and Mitochondria-Derived Reactive Oxygen Species in Cardioprotection of Ischemic Reperfusion Injury by Angiotensin II Hypertension, May 1, 2005; 45(5): 860 - 866. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
U. Laufs, S. Wassmann, T. Czech, T. Munzel, M. Eisenhauer, M. Bohm, and G. Nickenig Physical Inactivity Increases Oxidative Stress, Endothelial Dysfunction, and Atherosclerosis Arterioscler Thromb Vasc Biol, April 1, 2005; 25(4): 809 - 814. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. M. Pollock Endothelin, Angiotensin, and Oxidative Stress in Hypertension Hypertension, April 1, 2005; 45(4): 477 - 480. [Full Text] [PDF]
|
|
|
|
|
|
R. M. Touyz, C. Mercure, Y. He, D. Javeshghani, G. Yao, G. E. Callera, A. Yogi, N. Lochard, and T. L. Reudelhuber Angiotensin II-Dependent Chronic Hypertension and Cardiac Hypertrophy Are Unaffected by gp91phox-Containing NADPH Oxidase Hypertension, April 1, 2005; 45(4): 530 - 537. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Kimura, G.-X. Zhang, A. Nishiyama, T. Shokoji, L. Yao, Y.-Y. Fan, M. Rahman, and Y. Abe Mitochondria-Derived Reactive Oxygen Species and Vascular MAP Kinases: Comparison of Angiotensin II and Diazoxide Hypertension, March 1, 2005; 45(3): 438 - 444. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. K. Griendling ATVB In Focus: Redox Mechanisms in Blood Vessels Arterioscler Thromb Vasc Biol, February 1, 2005; 25(2): 272 - 273. [Full Text] [PDF]
|
|
|
|
|
|
C. S. Wilcox and D. Gutterman Focus on oxidative stress in the cardiovascular and renal systems Am J Physiol Heart Circ Physiol, January 1, 2005; 288(1): H3 - H6. [Full Text] [PDF]
|
|
|
|
|
|
N. R. Madamanchi, A. Vendrov, and M. S. Runge Oxidative Stress and Vascular Disease Arterioscler Thromb Vasc Biol, January 1, 2005; 25(1): 29 - 38. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.-M. Li and A. M Shah Endothelial cell superoxide generation: regulation and relevance for cardiovascular pathophysiology Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2004; 287(5): R1014 - R1030. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Engberding, S. Spiekermann, A. Schaefer, A. Heineke, A. Wiencke, M. Muller, M. Fuchs, D. Hilfiker-Kleiner, B. Hornig, H. Drexler, et al. Allopurinol Attenuates Left Ventricular Remodeling and Dysfunction After Experimental Myocardial Infarction: A New Action for an Old Drug? Circulation, October 12, 2004; 110(15): 2175 - 2179. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Stocker and J. F. Keaney Jr. Role of Oxidative Modifications in Atherosclerosis Physiol Rev, October 1, 2004; 84(4): 1381 - 1478. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Jin, Z. Ying, and R. C. Webb Activation of Rho/Rho kinase signaling pathway by reactive oxygen species in rat aorta Am J Physiol Heart Circ Physiol, October 1, 2004; 287(4): H1495 - H1500. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Fink, K. Laude, L. McCann, A. Doughan, D. G. Harrison, and S. Dikalov Detection of intracellular superoxide formation in endothelial cells and intact tissues using dihydroethidium and an HPLC-based assay Am J Physiol Cell Physiol, October 1, 2004; 287(4): C895 - C902. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Wassmann, K. Wassmann, and G. Nickenig Modulation of Oxidant and Antioxidant Enzyme Expression and Function in Vascular Cells Hypertension, October 1, 2004; 44(4): 381 - 386. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Chen, A.-P. Arrigo, and R. W. Currie Heat shock treatment suppresses angiotensin II-induced activation of NF-{kappa}B pathway and heart inflammation: a role for IKK depletion by heat shock? Am J Physiol Heart Circ Physiol, September 1, 2004; 287(3): H1104 - H1114. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. M. Touyz Reactive Oxygen Species, Vascular Oxidative Stress, and Redox Signaling in Hypertension: What Is the Clinical Significance? Hypertension, September 1, 2004; 44(3): 248 - 252. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. P. Brandes And What About the Endothelium?: On the Predominance of Cerebral Superoxide Formation for Angiotensin II-Induced Systemic Hypertension Circ. Res., July 23, 2004; 95(2): 122 - 124. [Full Text] [PDF]
|
|
|
|
|
|
M. C. Zimmerman, E. Lazartigues, R. V. Sharma, and R. L. Davisson Hypertension Caused by Angiotensin II Infusion Involves Increased Superoxide Production in the Central Nervous System Circ. Res., July 23, 2004; 95(2): 210 - 216. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Adachi, D. R. Pimentel, T. Heibeck, X. Hou, Y. J. Lee, B. Jiang, Y. Ido, and R. A. Cohen S-Glutathiolation of Ras Mediates Redox-sensitive Signaling by Angiotensin II in Vascular Smooth Muscle Cells J. Biol. Chem., July 9, 2004; 279(28): 29857 - 29862. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Z. Ungvari, A. Csiszar, P. M. Kaminski, M. S. Wolin, and A. Koller Chronic High Pressure-Induced Arterial Oxidative Stress: Involvement of Protein Kinase C-Dependent NAD(P)H Oxidase and Local Renin-Angiotensin System Am. J. Pathol., July 1, 2004; 165(1): 219 - 226. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Q. Liu and R. J. Folz Extracellular superoxide enhances 5-HT-induced murine pulmonary artery vasoconstriction Am J Physiol Lung Cell Mol Physiol, July 1, 2004; 287(1): L111 - L118. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K K Griendling Novel NAD(P)H oxidases in the cardiovascular system Heart, May 1, 2004; 90(5): 491 - 493. [Full Text] [PDF]
|
|
|
|
|
|
M. J. Ryan, S. P. Didion, S. Mathur, F. M. Faraci, and C. D. Sigmund Angiotensin II-Induced Vascular Dysfunction Is Mediated by the AT1A Receptor in Mice Hypertension, May 1, 2004; 43(5): 1074 - 1079. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.-M. Li, S. Wheatcroft, L. M. Fan, M. T. Kearney, and A. M. Shah Opposing Roles of p47phox in Basal Versus Angiotensin II-Stimulated Alterations in Vascular O2- Production, Vascular Tone, and Mitogen-Activated Protein Kinase Activation Circulation, March 16, 2004; 109(10): 1307 - 1313. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Werner GTPases and reactive oxygen species: switches for killing and signaling J. Cell Sci., January 15, 2004; 117(2): 143 - 153. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. S. McNally, M. E. Davis, D. P. Giddens, A. Saha, J. Hwang, S. Dikalov, H. Jo, and D. G. Harrison Role of xanthine oxidoreductase and NAD(P)H oxidase in endothelial superoxide production in response to oscillatory shear stress Am J Physiol Heart Circ Physiol, December 1, 2003; 285(6): H2290 - H2297. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Taniyama and K. K. Griendling Reactive Oxygen Species in the Vasculature: Molecular and Cellular Mechanisms Hypertension, December 1, 2003; 42(6): 1075 - 1081. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Hwang, A. Saha, Y. C. Boo, G. P. Sorescu, J. S. McNally, S. M. Holland, S. Dikalov, D. P. Giddens, K. K. Griendling, D. G. Harrison, et al. Oscillatory Shear Stress Stimulates Endothelial Production of O2- from p47phox-dependent NAD(P)H Oxidases, Leading to Monocyte Adhesion J. Biol. Chem., November 21, 2003; 278(47): 47291 - 47298. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Ritz and V. Haxsen Angiotensin II and Oxidative Stress: An Unholy Alliance J. Am. Soc. Nephrol., November 1, 2003; 14(11): 2985 - 2987. [Full Text] [PDF]
|
|
|
|
|
|
S. Fujii, L. Zhang, J. Igarashi, and H. Kosaka L-Arginine Reverses p47phox and gp91phox Expression Induced by High Salt in Dahl Rats Hypertension, November 1, 2003; 42(5): 1014 - 1020. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. K. Griendling and G. A. FitzGerald Oxidative Stress and Cardiovascular Injury: Part II: Animal and Human Studies Circulation, October 28, 2003; 108(17): 2034 - 2040. [Full Text] [PDF]
|
|
|
|
|
|
O. Jung, S. L. Marklund, H. Geiger, T. Pedrazzini, R. Busse, and R. P. Brandes Extracellular Superoxide Dismutase Is a Major Determinant of Nitric Oxide Bioavailability: In Vivo and Ex Vivo Evidence From ecSOD-Deficient Mice Circ. Res., October 3, 2003; 93(7): 622 - 629. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Gregg, F. M. Rauscher, and P. J. Goldschmidt-Clermont Rac regulates cardiovascular superoxide through diverse molecular interactions: more than a binary GTP switch Am J Physiol Cell Physiol, October 1, 2003; 285(4): C723 - C734. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Tepel Oxidative stress: does it play a role in the genesis of essential hypertension and hypertension of uraemia? Nephrol. Dial. Transplant., August 1, 2003; 18(8): 1439 - 1442. [Full Text] [PDF]
|
|
|
|
|
|
M. Tepel Oxidative stress: does it play a role in the genesis of essential hypertension and hypertension of uraemia? Nephrol. Dial. Transplant., August 1, 2003; 18(88): 1439 - 1442. [Full Text]
|
|
|
|
|
|
B. Lassegue and R. E. Clempus Vascular NAD(P)H oxidases: specific features, expression, and regulation Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2003; 285(2): R277 - R297. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Grote, I. Flach, M. Luchtefeld, E. Akin, S. M. Holland, H. Drexler, and B. Schieffer Mechanical Stretch Enhances mRNA Expression and Proenzyme Release of Matrix Metalloproteinase-2 (MMP-2) via NAD(P)H Oxidase-Derived Reactive Oxygen Species Circ. Res., June 13, 2003; 92 (11): e80 - e86. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. G Harrison, Hua Cai, U. Landmesser, and K. K Griendling The Pickering Lecture British Hypertension Society, 10th September 2002: Interactions of angiotensin II with NAD(P)H oxidase, oxidant stress and cardiovascular disease Journal of Renin-Angiotensin-Aldosterone System, June 1, 2003; 4(2): 51 - 61. [Abstract] [PDF]
|
|
|
|
|
|
M. J Brown A RATIONAL BASIS FOR SELECTION AMONG DRUGS OF THE SAME CLASS Heart, June 1, 2003; 89(6): 687 - 694. [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||