(Circulation. 1997;95:588-593.)
© 1997 American Heart Association, Inc.
Articles |
Role of Superoxide in Angiotensin II–Induced but Not Catecholamine-Induced Hypertension
the Department of Medicine, Cardiology Division, Emory University School of Medicine (J.B.L., S.R., Z.G., D.G.H.), Atlanta, Ga; the Atlanta (Ga) Veterans Administration Medical Center (D.G.H.); the Department of Anesthesiology (M.T., B.A.F.), University of Alabama at Birmingham; and Medical Department B, Division of Cardiology (J.B.L.), Rigshospitalet, Denmark.
Correspondence to David G. Harrison, MD, PO Box LL, Cardiology Division, Emory University School of Medicine, Atlanta, GA 30322.
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Abstract |
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Background The major source of superoxide (·O2-) in vascular tissues is an NADH/NADPH-dependent, membrane-bound oxidase. We have previously shown that this oxidase is activated in angiotensin II– but not norepinephrine-induced hypertension. We hypothesized that hypertension associated with chronically elevated angiotensin II might be caused in part by vascular ·O2- production.
Methods and Results We produced hypertension in rats by a 5-day infusion of angiotensin II or norepinephrine. Rats were also treated with liposome-encapsulated superoxide dismutase (SOD) or empty liposomes. Arterial pressure was measured in conscious rats under baseline conditions and during bolus injections of either acetylcholine or nitroprusside. Vascular ·O2- production was assessed by lucigenin chemiluminescence. In vitro vascular relaxations were examined in organ chambers. Norepinephrine infusion increased blood pressure to a similar extent as angiotensin II infusion (179±5 and 189±4 mm Hg, respectively). In contrast, angiotensin II–induced hypertension was associated with increased vascular ·O2- production, whereas norepinephrine-induced hypertension was not. Treatment with liposome-encapsulated SOD reduced blood pressure by 50 mm Hg in angiotensin II–infused rats while having no effect on blood pressure in control rats or rats with norepinephrine-induced hypertension. Similarly, liposome-encapsulated SOD enhanced in vivo hypotensive responses to acetylcholine and in vitro responses to endothelium-dependent vasodilators in angiotensin II–treated rats.
Conclusions Hypertension caused by chronically elevated angiotensin II is mediated in part by ·O2-, likely via degradation of endothelium-derived NO·. Increased vascular ·O2- may contribute to vascular disease in high renin/angiotensin II states.
Key Words: hypertension • angiotensin • endothelium-derived factors
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Introduction |
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It has become clear that both endothelial and vascular smooth muscle cells are capable of producing superoxide anions (·O2-) and other oxygen-derived radical metabolites of ·O2.1 2 3 4 5 6 A major source of ·O2- in vascular tissues is a membrane-bound oxidase that uses NADH predominantly as a substrate for electron donation to molecular oxygen.1 4 5 6 In cultured rat aortic vascular smooth muscle cells, the activity of this oxidase is increased by relatively low (0.1 to 100 nmol/L) concentrations of angiotensin II.7 More recently, we found that treatment of rats with angiotensin II for 5 days increases ·O2- production from aortic segments and increases NADH oxidase activity in aortic homogenates.8 This increase in vascular ·O2- production was associated with impaired endothelium-dependent relaxations to acetylcholine and the calcium ionophore A23187. In those studies, we found that norepinephrine infusion, which produced a similar degree of hypertension, did not increase vascular ·O2- production or vascular relaxations. These previous studies were performed in segments of conduit vessels. If angiotensin II had a similar effect in the resistance circulation, an increase in vascular ·O2- production might contribute to the hypertension caused by the peptide. We performed the present study to examine this hypothesis. Vascular superoxide dismutase (SOD) levels were increased by daily injections of liposome-entrapped SOD. The effect of this treatment on blood pressure in control rats and rats with either norepinephrine- or angiotensin II–induced hypertension was examined.
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Methods |
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Liposome-Entrapped SOD
Liposomes were composed of dioleoyl-phosphatidylethanolamine and dioleoyl-glycero-3-succinate (1:1; Avanti Polar Lipids). Lipids were dried under N2 and hydrated 36 hours in 210 mmol/L sucrose and 7 mmol/L HEPES. During hydration, pH 8.5 was maintained with tetraethylammonium hydroxide (Sigma Chemical Co). Lipids were added to CuZn SOD (Diagnostic Data Inc) and dissolved in sucrose-HEPES buffer, and the mixture was extruded through a 600-nm filter under N2· pressure (Extruder, Lipex Biomembranes); mean liposome diameter was 217 nm.
Animal Preparation
Catheters were implanted for drug administration and blood pressure measurements in male Sprague-Dawley rats as described before.9 The rats were treated with daily injections of either empty liposomes or liposome-entrapped SOD (1000 U).
Three days after the start of treatment with liposome-entrapped SOD or empty liposomes (day 3), osmotic minipumps containing either angiotensin II (0.7 mg·kg-1·d-1, treatment group 1), norepinephrine (2.8 mg·kg-1·d-1, treatment group 2), or vehicle (NaCl, treatment group 3) were implanted as previously described.8
Arterial Pressure Measurements
The animals were handled daily and exposed to the environment eventually used for blood pressure measurement. On the fifth day of osmotic minipump treatment (day 8), the mean arterial blood pressure (MAP) was measured while the animals were conscious. In addition, blood pressure responses to either acetylcholine (40 µg/kg) or sodium nitroprusside (80 µg/kg) were measured as described previously.9 These doses were selected on the basis of preliminary dose-response curves to elicit a fall in MAP of 
35 mm Hg (30 to 40 mm Hg) in normal untreated rats. In preliminary experiments, the effect of acetylcholine was completely inhibited by pretreatment with 120 mg/kg L-N-monomethyl arginine, indicating that the hypotensive effect of a bolus of acetylcholine was due to the activation of NO synthase.
In Vitro Vessel Studies
Vessels were studied in organ chambers by the use of methods described previously.8 Superoxide (·O2-) production was measured by the use of lucigenin chemiluminescence. The details of this assay have been published previously.10 11
Determination of SOD Enzyme Activity
Aortas were homogenized with a Dounce homogenizer in a 50 mmol/L potassium phosphate buffer. SOD activity was determined spectrophotometrically by the ability of the homogenate (50 µg total protein) to inhibit reduction of ferricytochrome c by the superoxide anion generated by the addition of xanthine and xanthine oxidase. Values obtained were represented as units of SOD per milligram of protein. Calibrations were performed with the use of known amounts of purified bovine SOD.
Detection of Macrophages by Immunocytochemistry
Rat macrophages were identified by immunofluorescent staining with the use of a purified monoclonal antibody (PharMingen) recognizing an ED-2–like antigen on rat tissue macrophages.12 Rat aortas were harvested from three control and three 5-day angiotensin II–treated rats. Specimens of rat spleen and lungs were also collected and processed as positive controls. Tissues were embedded in OCT (Miles) and frozen in liquid nitrogen. Primary and secondary antibodies were diluted with 50 mmol/L Tris-HCl, pH 7.2, containing 1 mg/mL bovine serum albumin (wash buffer) supplemented with 10% horse serum. Frozen tissue sections (8 µm) were fixed for 5 minutes with cold acetone (-20°C). Nonspecific staining was blocked by incubating the sections for 5 minutes with 10% horse serum, then sections were incubated with anti-rat macrophage antibody (1/200) for 1 hour. After rinsing and washing with wash buffer, sections were incubated for 30 minutes with Affinipure donkey anti-mouse IgG antibodies (affinity adsorbed with rat serum proteins to prevent cross-reaction; Jackson ImmunoResearch) coupled to Texas Red or fluorescein isothiocyanate (FITC). Some of the specimens were processed without the primary antibody as negative controls. Cell nuclei were stained with 0.5 µg/mL bis-benzimide (Calbiochem) in PBS for 2 minutes. Specimens were observed and photographed with a Zeiss Axioskop microscope equipped with a triple-fluorescence filter.
Data Analysis
Data are expressed as mean±SEM. Comparisons between groups were made by use of one-way ANOVA. When significance was indicated, a Student-Newman-Keuls post hoc analysis was used. To examine interactions between angiotensin II or sham treatment and liposome-encapsulated SOD treatment, a two-way ANOVA was used, in which either sham or angiotensin II treatment was one independent variable and either empty liposomes or liposome-encapsulated SOD was the other independent variable. Significance was considered present when the probability value was <.05.
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Results |
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Effect of Liposome-Encapsulated SOD Treatment on Vascular SOD Activity
In all three groups of rats, liposome-entrapped SOD increased total SOD activity by
30% (Fig 1
).
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Vascular Superoxide Production
Lucigenin counts from aortic segments of control rats receiving empty liposomes averaged 3.0±0.5·103 counts·min-1·mg-1. Treatment with liposome-encapsulated SOD did not alter this value in controls (Fig 2). Superoxide production, as assessed by lucigenin-enhanced chemiluminescence, was increased threefold in vascular segments from angiotensin II–infused rats treated with empty liposomes (P<.05 versus control). Liposome-entrapped SOD normalized ·O2- production in vessels from angiotensin II–treated rats. In contrast to angiotensin II treatment, and in agreement with our previous study, norepinephrine infusion did not affect vascular ·O2- production (Fig 2).
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Effect of Liposome-Encapsulated SOD on MAP in Angiotensin II– and Norepinephrine-Treated Animals
MAP was not different between animals receiving either liposome-encapsulated SOD or empty liposomes in either controls or norepinephrine-infused rats (Fig 3; P>.05). In contrast, treatment with liposome-entrapped SOD for 8 consecutive days markedly decreased the hypertension caused by angiotensin II (P<.05; Fig 3).
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Effect of Encapsulated SOD on In Vivo Responses to Acetylcholine and Sodium Nitroprusside
In control and angiotensin II–infused animals, liposome-entrapped treatment increased the hypotensive responses to acetylcholine, whether expressed as an absolute change in pressure or as a percent change in arterial pressure (Table 1). In contrast, treatment with liposome-encapsulated SOD had no effect on the hypotensive response to acetylcholine in the rats treated with norepinephrine.
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Responses to sodium nitroprusside were not altered by treatment with liposome-encapsulated SOD (Table 2).
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In Vitro Vascular Relaxations
In normal vessels from animals treated with empty liposomes, relaxations to acetylcholine were 86±3%. Treatment with liposome-entrapped SOD increased these to 98±2%. In angiotensin II–treated rats that had received empty liposomes, maximal relaxations to acetylcholine were markedly reduced compared with control rings (37±6%). Treatment of angiotensin II–infused animals with liposome-entrapped SOD substantially enhanced maximal relaxations to acetylcholine (Fig 4a; Table 3). Sensitivity to acetylcholine, as reflected by the ED50s, was likewise increased in both control and angiotensin II–treated animals by long-term administration of liposome-encapsulated SOD. In control rats, the calcium ionophore A23187 produced relaxations averaging 86±7% and 100±1% of the preconstricted tension in the empty liposome and liposome-encapsulated SOD groups, respectively. In vessels from angiotensin II–treated animals, relaxations to the calcium ionophore were significantly impaired in the empty-liposome group (58±7%). In the angiotensin II–treated animals, administration of liposome-encapsulated SOD markedly enhanced relaxations to A23187 (Table 3; Fig 4b).
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In control vessels, nitroglycerin produced maximal relaxations of 99±1% and 97±3% in the empty-liposome and liposome-encapsulated SOD groups, respectively. In vessels from angiotensin II–infused rats treated with empty liposomes, relaxations evoked by nitroglycerin were significantly impaired compared with relaxations in the control vessels (68±8%). These were substantially enhanced by treatment with liposome-encapsulated SOD. ED50s to nitroglycerin were similar in the angiotensin II and control animals. In both groups, treatment with liposome-encapsulated SOD lowered the ED50 (Table 3
; Fig 4c).
Two-way ANOVA indicated that the effect of liposome-encapsulated SOD on peak relaxations in response to acetylcholine, calcium ionophore A23187, and nitroglycerin was greater in the rats with angiotensin II–induced hypertension than in controls.
Macrophage Content in Aortas of Control and Angiotensin II–Treated Rats
Anti-macrophage antibodies stained isolated cells in the adventitia in both the control and the angiotensin II–treated rats. There was no obvious difference between adventitial staining in the two groups. Positive control specimens for the anti-rat macrophage antibody showed staining of white pulp macrophages in the spleen and alveolar macrophages in the lungs. Only background fluorescence was observed in sections in which the primary antibody was not added (data not shown).
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Discussion |
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In the present study, we found that increasing vascular SOD levels by daily injection of liposome-entrapped SOD attenuated the rise in blood pressure by
50 mm Hg in rats with angiotensin II–induced hypertension. Liposome-entrapped SOD treatment also enhanced the in vivo hypotensive effect of intravenous acetylcholine and increased in vitro relaxations to acetylcholine, the calcium ionophore A23187, and nitroglycerin. The blood pressure–lowering effect of liposome-encapsulated SOD was not observed in norepinephrine-induced hypertension. In this latter model, ·O2- production by larger conduit vessels was not increased. These findings confirm a recent study from our laboratory8 showing that angiotensin II–induced but not norepinephrine-induced hypertension was associated with an increase in vascular ·O2- production and an alteration in endothelium-dependent vascular relaxation. The present findings suggest that the effect of angiotensin II to increase vascular ·O2- production extends to the resistance circulation, which is involved in blood pressure control. These findings are also in keeping with a previously published report14 showing that a recombinant form of SOD that would bind to vascular glycosaminoglycans could acutely lower blood pressure in spontaneously hypertensive rats when injected intravenously. In the report by Nakazono et al,14 the effect of the recombinant SOD was short-lived. In contrast, we found that long-term treatment with liposome-encapsulated SOD produced a sustained decrease in blood pressure. Our findings also extend those of Nakazono et al14 in that we demonstrated that this effect of SOD did not occur in catecholamine-induced hypertension. We hypothesize that forms of hypertension associated with elevated levels of either circulating or local angiotensin II (which can activate vascular membrane oxidases) would more likely be susceptible to treatment with SOD.
Treatment with liposome-entrapped SOD did not completely correct hypertension in the angiotensin II–treated rats. Whether a higher dose of SOD might have proven more beneficial remains unknown; however, it is almost certain that mechanisms independent of ·O2- are important in this form of hypertension. Furthermore, changes in the morphology of resistance vessels may contribute importantly to hypertension in the setting of elevations of angiotensin II.
In our previous study,8 we found that the source of the increase in ·O2- in rats with angiotensin II–induced hypertension was likely an NADH-dependent oxidase. This oxidase has been shown7 to be the predominant source of ·O2- in the vessel wall and recently was found to be activated by angiotensin II in cultured vascular smooth muscle cells. In the present study, because of the small size of the resistance vessels involved, we could not characterize the oxidase involved, but we assume it is similar to that activated in the larger vessels.
One consideration is that macrophages in the vessel wall contribute to the increase in vascular ·O2- production. This seems unlikely for two reasons. First, in our previous study,8 we found the predominant oxidase in aortas of these animals was NADH dependent, whereas the macrophage oxidase is NADPH dependent. Second, in the present study, we found a small number of macrophages were scattered about the adventitia in both groups of vessels, and no macrophages were observed in the media or subintimal space. Although this immunohistochemical approach is only semiquantitative, we were unable to detect a difference in the number of macrophages present in the two vessel types.
It is likely that the increase in ·O2- production in the setting of angiotensin II–induced hypertension results in diversion of locally released NO· to nitrite, nitrate, and the peroxynitrite anion. Inorganic nitrite and nitrate are not vasoactive, except in very high (>100 µmol/L) concentrations. Peroxynitrite is a highly reactive molecule implicated in lipid peroxidation and cellular injury.15 16 17 18 Peroxynitrite is capable of producing vasodilation,19 likely via formation of nitric oxide–donating species.20 Direct comparisons between peroxynitrite and NO· indicate that NO· is 100 to 1000 times more potent than peroxynitrite in its ability to increase cGMP.21 Liposome-entrapped SOD treatment likely limited this interaction between ·O2- and NO· and thus preserved the vasodilator effect. This conclusion is supported by our findings that liposome-entrapped SOD treatment substantially enhanced endothelium-dependent vascular relaxations and relaxations to exogenous vasodilators. It has been suggested that an important product of the endothelial NO synthase is the nitroxyl anion (NO-)22 and that nitroxyl can be converted to NO· by SOD. Thus, another mechanism by which liposome-entrapped SOD might lower blood pressure is increased formation of NO· from nitroxyl, although this might have been expected to occur in all groups of animals studied.23 Finally, it has also been suggested that ·O2- itself can serve as a vasoconstrictor agent.1 It is therefore possible that the blood pressure–lowering effect of the liposome-encapsulated SOD might be simply due to reduction of ·O2- levels independent of an effect on NO·.
Liposome-entrapped SOD was used in the present study to augment vascular SOD levels. In previous studies, native SOD has been shown to penetrate poorly into endothelial cells, and when injected intravenously, it does not augment tissue levels of SOD.24 25 Furthermore, we11 have found that native SOD, when added directly to a vessel in an organ chamber, has a minimal effect on vascular relaxations to endothelium-dependent vasodilators or to exogenous nitrovasodilators. Likewise, in preliminary studies, we found that intravenous administration of native SOD had little effect on in vivo responses to nitrovasodilators or acetylcholine. Native SOD is negatively charged and is therefore electrostatically repelled from the surface of vascular cells. The delivery of SOD via liposomes overcomes hindrances to vascular delivery. Recent studies26 have shown that intravenous injections of liposome-encapsulated SOD improve endothelium-dependent vascular relaxation in vessels from rabbits with diet-induced atherosclerosis.
The increase in vascular levels of SOD achieved by liposome-encapsulated SOD treatment averaged 30%. Although this may seem modest, when ambient levels of ·O2- are low, even small increases in SOD can markedly shorten the half-life of ·O2-.27 Therefore, the degree of increase in SOD achieved in the present studies may importantly modulate total vascular ·O2- levels. This was confirmed by our estimates of vascular ·O2- production using lucigenin-enhanced chemiluminescence. Furthermore, the localization of the liposome-delivered SOD may be important. Previous studies using electron micrographic localization have revealed endothelial cell, smooth muscle cell, and interstitial delivery of SOD. In particular, interstitial delivery may be quite important in preventing degradation of NO· because it traverses interstitial spaces.
To examine the consequences of ·O2- scavenging in vivo, we examined responses to an intravenous bolus of acetylcholine. Because these studies were performed in vivo while the animals were conscious, it was difficult to perform a detailed dose-response curve to acetylcholine in all animals. In preliminary studies, however, a dose-response curve was performed in control animals, and the dose selected (40 µg/kg) was found to produce an intermediate hypotensive response. This was selected to avoid excessive hypotension in controls and to allow detection of differences between the controls and the hypertensive animals. The augmented hypotensive response to acetylcholine in the liposome-encapsulated SOD–treated animals suggests that the levels of SOD were augmented in the microcirculation as well as in the larger conduit vessels.
Treatment with liposome-entrapped SOD enhanced the blood pressure response to acetylcholine not only in rats with angiotensin II–induced hypertension but also in controls. This finding is again compatible with the concept that even in the normal situation, a balance exists between NO· and ·O2- that importantly influences responsiveness of vessels in the microcirculation to endothelium-dependent vasodilators.
Treatment with liposome-entrapped SOD did not affect the blood pressure response to acetylcholine in the norepinephrine-treated rats. Although this observation is at first difficult to understand, there are complex interactions between norepinephrine and acetylcholine that may make interpretation of these findings difficult. For example, 
-adrenergic stimulation has been shown to enhance acetylcholine release in brain slices28 and perfused rat hearts.29 If this occurred in vivo, downregulation of muscarinic receptors might result, leading to a relative loss of responsiveness to acetylcholine in these animals.
Beyond simply enhancing the effects of nitric oxide, there are other potential mechanisms whereby liposome-entrapped SOD could prevent the hypertension caused by angiotensin II. These include alterations of baroreceptor responsiveness, interactions with other neurohumoral influences, and changes in blood volume. It has been observed, for example, that nitric oxide can modulate baroreflex activity.30 Likewise, angiotensin II has been shown to stimulate the production of endothelin-1 by vascular smooth muscle.31 Whether or not these interactions could be modified by ·O2-, other reactive oxygen species, or SOD requires further investigation. Additionally, liposome-entrapped SOD, owing to its lipophilic character, could cross the blood-brain barrier and exert central effects.
These findings may provide insight into the clinical observations that hypertensive populations with elevated renin profiles (and presumably, elevated angiotensin II) have an increase in cardiovascular event rates compared with groups of hypertensive subjects with low renin profiles.32 Superoxide anion and its oxygen radical metabolites can not only alter endothelium-dependent vascular relaxation but may also participate in the oxidation of LDLs,33 the activation of proto-oncogenes and the promotion of cellular growth,34 35 and the activation of proinflammatory molecules, such as the vascular cell-adhesion molecule.36 Many of these properties are shared by angiotensin II,37 38 39 40 and at least one mechanism responsible for vascular disease in angiotensin II–induced hypertension is increased production of ·O2-.
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Acknowledgments |
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This work was supported by National Institutes of Health grants HL-39006 and DK-45215, a merit review grant from the Veterans Administration, and Vascular Biology Program Project grants HL-48667 and HL-48676. Dr Tarpey is a recipient of an NIH Clinician Investigator Award. Dr Bech Laursen is supported by grants from the Danish Heart Foundation, the Jørgen Møller Foundation, and Bristol-Meyers Squibb A/S, Denmark.
Received February 26, 1996; revision received September 11, 1996; accepted September 30, 1996.
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 P. Mathieu, P. Poirier, P. Pibarot, I. Lemieux, and J.-P. Despres Visceral Obesity: The Link Among Inflammation, Hypertension, and Cardiovascular Disease Hypertension, April 1, 2009; 53(4): 577 - 584. [Full Text] [PDF]
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 K. K. Koh, P. C. Oh, and M. J. Quon Does reversal of oxidative stress and inflammation provide vascular protection? Cardiovasc Res, March 1, 2009; 81(4): 649 - 659. [Abstract] [Full Text] [PDF]
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 C. S. Wilcox and A. Pearlman Chemistry and Antihypertensive Effects of Tempol and Other Nitroxides Pharmacol. Rev., December 1, 2008; 60(4): 418 - 469. [Abstract] [Full Text] [PDF]
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Z. Qin, M. C. Gongora, K. Ozumi, S. Itoh, K. Akram, M. Ushio-Fukai, D. G. Harrison, and T. Fukai Role of Menkes ATPase in Angiotensin II-Induced Hypertension: A Key Modulator for Extracellular Superoxide Dismutase Function Hypertension, November 1, 2008; 52(5): 945 - 951. [Abstract] [Full Text] [PDF]
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B. Xue, Y. Zhao, A. K. Johnson, and M. Hay Central estrogen inhibition of angiotensin II-induced hypertension in male mice and the role of reactive oxygen species Am J Physiol Heart Circ Physiol, September 1, 2008; 295(3): H1025 - H1032. [Abstract] [Full Text] [PDF]
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A. Lopez-Ruiz, J. Sartori-Valinotti, L. L. Yanes, R. Iliescu, and J. F. Reckelhoff Sex differences in control of blood pressure: role of oxidative stress in hypertension in females Am J Physiol Heart Circ Physiol, August 1, 2008; 295(2): H466 - H474. [Abstract] [Full Text] [PDF]
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A. Just, C. L. Whitten, and W. J. Arendshorst Reactive oxygen species participate in acute renal vasoconstrictor responses induced by ETA and ETB receptors Am J Physiol Renal Physiol, April 1, 2008; 294(4): F719 - F728. [Abstract] [Full Text] [PDF]
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N. G. Abraham and A. Kappas Pharmacological and Clinical Aspects of Heme Oxygenase Pharmacol. Rev., March 1, 2008; 60(1): 79 - 127. [Abstract] [Full Text] [PDF]
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Z. V. Wang and P. E. Scherer Adiponectin, Cardiovascular Function, and Hypertension Hypertension, January 1, 2008; 51(1): 8 - 14. [Full Text] [PDF]
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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]
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S. A. Cooper, A. Whaley-Connell, J. Habibi, Y. Wei, G. Lastra, C. Manrique, S. Stas, and J. R. Sowers Renin-angiotensin-aldosterone system and oxidative stress in cardiovascular insulin resistance Am J Physiol Heart Circ Physiol, October 1, 2007; 293(4): H2009 - H2023. [Abstract] [Full Text] [PDF]
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Y. Chen, A. Pearlman, Z. Luo, and C. S. Wilcox Hydrogen peroxide mediates a transient vasorelaxation with tempol during oxidative stress Am J Physiol Heart Circ Physiol, October 1, 2007; 293(4): H2085 - H2092. [Abstract] [Full Text] [PDF]
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L. Ding, A. Chapman, R. Boyd, and H. D. Wang ERK activation contributes to regulation of spontaneous contractile tone via superoxide anion in isolated rat aorta of angiotensin II-induced hypertension Am J Physiol Heart Circ Physiol, June 1, 2007; 292(6): H2997 - H3005. [Abstract] [Full Text] [PDF]
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S. M. Zemse, R. H. P. Hilgers, and R. C. Webb Interleukin-10 counteracts impaired endothelium-dependent relaxation induced by ANG II in murine aortic rings Am J Physiol Heart Circ Physiol, June 1, 2007; 292(6): H3103 - H3108. [Abstract] [Full Text] [PDF]
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R. H. P. Hilgers and R. C. Webb Reduced expression of SKCa and IKCa channel proteins in rat small mesenteric arteries during angiotensin II-induced hypertension Am J Physiol Heart Circ Physiol, May 1, 2007; 292(5): H2275 - H2284. [Abstract] [Full Text] [PDF]
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Z. Wang, I. Armando, L. D. Asico, C. Escano, X. Wang, Q. Lu, R. A. Felder, C. G. Schnackenberg, D. R. Sibley, G. M. Eisner, et al. The elevated blood pressure of human GRK4{gamma} A142V transgenic mice is not associated with increased ROS production Am J Physiol Heart Circ Physiol, May 1, 2007; 292(5): H2083 - H2092. [Abstract] [Full Text] [PDF]
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K.-T. Kang, J. C. Sullivan, J. M. Sasser, J. D. Imig, and J. S. Pollock Novel Nitric Oxide Synthase-Dependent Mechanism of Vasorelaxation in Small Arteries From Hypertensive Rats Hypertension, April 1, 2007; 49(4): 893 - 901. [Abstract] [Full Text] [PDF]
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 D. Wang, P. Jose, and C. S. Wilcox beta1 Receptors Protect the Renal Afferent Arteriole of Angiotensin-Infused Rabbits from Norepinephrine-Induced Oxidative Stress J. Am. Soc. Nephrol., December 1, 2006; 17(12): 3347 - 3354. [Abstract] [Full Text] [PDF]
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W. J. Welch, T. Chabrashvili, G. Solis, Y. Chen, P. S. Gill, S. Aslam, X. Wang, H. Ji, K. Sandberg, P. Jose, et al. Role of Extracellular Superoxide Dismutase in the Mouse Angiotensin Slow Pressor Response Hypertension, November 1, 2006; 48(5): 934 - 941. [Abstract] [Full Text] [PDF]
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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]
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M. C. Gongora, Z. Qin, K. Laude, H. W. Kim, L. McCann, J. R. Folz, S. Dikalov, T. Fukai, and D. G. Harrison Role of Extracellular Superoxide Dismutase in Hypertension Hypertension, September 1, 2006; 48(3): 473 - 481. [Abstract] [Full Text] [PDF]
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T. M. Paravicini and R. M. Touyz Redox signaling in hypertension Cardiovasc Res, July 15, 2006; 71(2): 247 - 258. [Abstract] [Full Text] [PDF]
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 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]
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 A. C. Grobe, S. M. Wells, E. Benavidez, P. Oishi, A. Azakie, J. R. Fineman, and S. M. Black Increased oxidative stress in lambs with increased pulmonary blood flow and pulmonary hypertension: role of NADPH oxidase and endothelial NO synthase Am J Physiol Lung Cell Mol Physiol, June 1, 2006; 290(6): L1069 - L1077. [Abstract] [Full Text] [PDF]
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 E. M. V. de Cavanagh, J. E. Toblli, L. Ferder, B. Piotrkowski, I. Stella, and F. Inserra Renal mitochondrial dysfunction in spontaneously hypertensive rats is attenuated by losartan but not by amlodipine Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2006; 290(6): R1616 - R1625. [Abstract] [Full Text] [PDF]
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L. Hao, T. Nishimura, H. Wo, and C. Fernandez-Patron Vascular Responses to {alpha}1-Adrenergic Receptors in Small Rat Mesenteric Arteries Depend on Mitochondrial Reactive Oxygen Species Arterioscler Thromb Vasc Biol, April 1, 2006; 26(4): 819 - 825. [Abstract] [Full Text] [PDF]
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X. Dai, X. Cao, and D. L. Kreulen Superoxide anion is elevated in sympathetic neurons in DOCA-salt hypertension via activation of NADPH oxidase Am J Physiol Heart Circ Physiol, March 1, 2006; 290(3): H1019 - H1026. [Abstract] [Full Text] [PDF]
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C. S. Packer Soluble guanylate cyclase (sGC) down-regulation by abnormal extracellular matrix proteins as a novel mechanism in vascular dysfunction: Implications in metabolic syndrome Cardiovasc Res, February 1, 2006; 69(2): 302 - 303. [Full Text] [PDF]
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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]
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A. Vidal, Y. Sun, S. K. Bhattacharya, R. A. Ahokas, I. C. Gerling, and K. T. Weber Calcium paradox of aldosteronism and the role of the parathyroid glands Am J Physiol Heart Circ Physiol, January 1, 2006; 290(1): H286 - H294. [Abstract] [Full Text] [PDF]
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K. Patel, Y. Chen, K. Dennehy, J. Blau, S. Connors, M. Mendonca, M. Tarpey, M. Krishna, J. B. Mitchell, W. J. Welch, et al. Acute antihypertensive action of nitroxides in the spontaneously hypertensive rat Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2006; 290(1): R37 - R43. [Abstract] [Full Text] [PDF]
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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]
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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]
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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]
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C. De Ciuceis, F. Amiri, P. Brassard, D. H. Endemann, R. M. Touyz, and E. L. Schiffrin Reduced Vascular Remodeling, Endothelial Dysfunction, and Oxidative Stress in Resistance Arteries of Angiotensin II-Infused Macrophage Colony-Stimulating Factor-Deficient Mice: Evidence for a Role in Inflammation in Angiotensin-Induced Vascular Injury Arterioscler Thromb Vasc Biol, October 1, 2005; 25(10): 2106 - 2113. [Abstract] [Full Text] [PDF]
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Y. Zhang, K. K. Griendling, A. Dikalova, G. K. Owens, and W. R. Taylor Vascular Hypertrophy in Angiotensin II-Induced Hypertension Is Mediated by Vascular Smooth Muscle Cell-Derived H2O2 Hypertension, October 1, 2005; 46(4): 732 - 737. [Abstract] [Full Text] [PDF]
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 R. Estelles, L. Milian, Y. N. A. Nabah, T. Mateo, M. Cerda-Nicolas, M. Losada, M. D. Ivorra, A. C. Issekutz, J. Cortijo, E. J. Morcillo, et al. Effect of boldine, secoboldine, and boldine methine on angiotensin II-induced neurtrophil recruitment in vivo J. Leukoc. Biol., September 1, 2005; 78(3): 696 - 704. [Abstract] [Full Text] [PDF]
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V. M. Campese, Y. Shaohua, and Z. Huiquin Oxidative Stress Mediates Angiotensin II-Dependent Stimulation of Sympathetic Nerve Activity Hypertension, September 1, 2005; 46(3): 533 - 539. [Abstract] [Full Text] [PDF]
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 Y.-L. Li, Y.-F. Li, D. Liu, K. G. Cornish, K. P. Patel, I. H. Zucker, K. M. Channon, and H. D. Schultz Gene Transfer of Neuronal Nitric Oxide Synthase to Carotid Body Reverses Enhanced Chemoreceptor Function in Heart Failure Rabbits Circ. Res., August 5, 2005; 97(3): 260 - 267. [Abstract] [Full Text] [PDF]
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A. Csiszar, K. E. Smith, A. Koller, G. Kaley, J. G. Edwards, and Z. Ungvari Regulation of Bone Morphogenetic Protein-2 Expression in Endothelial Cells: Role of Nuclear Factor-{kappa}B Activation by Tumor Necrosis Factor-{alpha}, H2O2, and High Intravascular Pressure Circulation, May 10, 2005; 111(18): 2364 - 2372. [Abstract] [Full Text] [PDF]
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B. T. Andresen, K. Shome, E. K. Jackson, and G. G. Romero AT2 receptors cross talk with AT1 receptors through a nitric oxide- and RhoA-dependent mechanism resulting in decreased phospholipase D activity Am J Physiol Renal Physiol, April 1, 2005; 288(4): F763 - F770. [Abstract] [Full Text] [PDF]
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I. Drenjancevic-Peric and J. H. Lombard Reduced Angiotensin II and Oxidative Stress Contribute to Impaired Vasodilation in Dahl Salt-Sensitive Rats on Low-Salt Diet Hypertension, April 1, 2005; 45(4): 687 - 691. [Abstract] [Full Text] [PDF]
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O. Suda, L. A. Smith, L. V. d'Uscio, T. E. Peterson, and Z. S. Katusic In Vivo Expression of Recombinant Vascular Endothelial Growth Factor in Rabbit Carotid Artery Increases Production of Superoxide Anion Arterioscler Thromb Vasc Biol, March 1, 2005; 25(3): 506 - 511. [Abstract] [Full Text] [PDF]
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 M. C. Blendea, D. Jacobs, C. S. Stump, S. I. McFarlane, C. Ogrin, G. Bahtyiar, S. Stas, P. Kumar, Q. Sha, C. M. Ferrario, et al. Abrogation of oxidative stress improves insulin sensitivity in the Ren-2 rat model of tissue angiotensin II overexpression Am J Physiol Endocrinol Metab, February 1, 2005; 288(2): E353 - E359. [Abstract] [Full Text] [PDF]
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B. Somoza, M. C. Gonzalez, J. M. Gonzalez, F. Abderrahim, S. M. Arribas, and M. S. Fernandez-Alfonso Modulatory role of the adventitia on noradrenaline and angiotensin II responses: Role of endothelium and AT2 receptors Cardiovasc Res, February 1, 2005; 65(2): 478 - 486. [Abstract] [Full Text] [PDF]
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A. A. Elmarakby, E. D. Loomis, J. S. Pollock, and D. M. Pollock NADPH Oxidase Inhibition Attenuates Oxidative Stress but Not Hypertension Produced by Chronic ET-1 Hypertension, February 1, 2005; 45(2): 283 - 287. [Abstract] [Full Text] [PDF]
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W. J. Welch, J. Blau, H. Xie, T. Chabrashvili, and C. S. Wilcox Angiotensin-induced defects in renal oxygenation: role of oxidative stress Am J Physiol Heart Circ Physiol, January 1, 2005; 288(1): H22 - H28. [Abstract] [Full Text] [PDF]
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R. P. Brandes and J. Kreuzer Vascular NADPH oxidases: molecular mechanisms of activation Cardiovasc Res, January 1, 2005; 65(1): 16 - 27. [Abstract] [Full Text] [PDF]
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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]
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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]
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M. C. Zimmerman, R. P. Dunlay, E. Lazartigues, Y. Zhang, R. V. Sharma, J. F. Engelhardt, and R. L. Davisson Requirement for Rac1-Dependent NADPH Oxidase in the Cardiovascular and Dipsogenic Actions of Angiotensin II in the Brain Circ. Res., September 3, 2004; 95(5): 532 - 539. [Abstract] [Full Text] [PDF]
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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]
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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]
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T. Matsumoto, H. Takashima, N. Ohira, Y. Tarutani, Y. Yasuda, T. Yamane, S. Matsuo, and M. Horie Plasma level of oxidized low-density lipoprotein is an independent determinant of coronary macrovasomotor and microvasomotor responses induced by bradykinin J. Am. Coll. Cardiol., July 21, 2004; 44(2): 451 - 457. [Abstract] [Full Text] [PDF]
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D. Wang, T. Chabrashvili, and C. S. Wilcox Enhanced Contractility of Renal Afferent Arterioles From Angiotensin-Infused Rabbits: Roles of Oxidative Stress, Thromboxane Prostanoid Receptors, and Endothelium Circ. Res., June 11, 2004; 94(11): 1436 - 1442. [Abstract] [Full Text] [PDF]
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S. Keidar, M. Kaplan, E. Pavlotzky, R. Coleman, T. Hayek, S. Hamoud, and M. Aviram Aldosterone Administration to Mice Stimulates Macrophage NADPH Oxidase and Increases Atherosclerosis Development: A Possible Role for Angiotensin-Converting Enzyme and the Receptors for Angiotensin II and Aldosterone Circulation, May 11, 2004; 109(18): 2213 - 2220. [Abstract] [Full Text] [PDF]
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J. R. Sowers Insulin resistance and hypertension Am J Physiol Heart Circ Physiol, May 1, 2004; 286(5): H1597 - H1602. [Abstract] [Full Text] [PDF]
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O. Jung, J.G. Schreiber, H. Geiger, T. Pedrazzini, R. Busse, and R.P. Brandes gp91phox-Containing NADPH Oxidase Mediates Endothelial Dysfunction in Renovascular Hypertension Circulation, April 13, 2004; 109(14): 1795 - 1801. [Abstract] [Full Text] [PDF]
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B. Rodriguez-Iturbe, N. D. Vaziri, J. Herrera-Acosta, and R. J. Johnson Oxidative stress, renal infiltration of immune cells, and salt-sensitive hypertension: all for one and one for all Am J Physiol Renal Physiol, April 1, 2004; 286(4): F606 - F616. [Abstract] [Full Text] [PDF]
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I. Eskurza, K. D. Monahan, J. A. Robinson, and D. R. Seals Ascorbic acid does not affect large elastic artery compliance or central blood pressure in young and older men Am J Physiol Heart Circ Physiol, April 1, 2004; 286(4): H1528 - H1534. [Abstract] [Full Text] [PDF]
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K. T. Weber From Inflammation to Fibrosis: A Stiff Stretch of Highway Hypertension, April 1, 2004; 43(4): 716 - 719. [Full Text] [PDF]
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W. Ni, S. Kitamoto, M. Ishibashi, M. Usui, S. Inoue, K.-i. Hiasa, Q. Zhao, K.-i. Nishida, A. Takeshita, and K. Egashira Monocyte Chemoattractant Protein-1 Is an Essential Inflammatory Mediator in Angiotensin II-Induced Progression of Established Atherosclerosis in Hypercholesterolemic Mice Arterioscler Thromb Vasc Biol, March 1, 2004; 24(3): 534 - 539. [Abstract] [Full Text]
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M. Galinanes and A. G Fowler Role of clinical pathologies in myocardial injury following ischaemia and reperfusion Cardiovasc Res, February 15, 2004; 61(3): 512 - 521. [Abstract] [Full Text] [PDF]
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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]
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T. Munzel, R. Feil, A. Mulsch, S. M. Lohmann, F. Hofmann, and U. Walter Physiology and Pathophysiology of Vascular Signaling Controlled by Cyclic Guanosine 3',5'-Cyclic Monophosphate-Dependent Protein Kinase Circulation, November 4, 2003; 108(18): 2172 - 2183. [Full Text] [PDF]
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C. Kitiyakara, T. Chabrashvili, Y. Chen, J. Blau, A. Karber, S. Aslam, W. J. Welch, and C. S. Wilcox Salt Intake, Oxidative Stress, and Renal Expression of NADPH Oxidase and Superoxide Dismutase J. Am. Soc. Nephrol., November 1, 2003; 14(11): 2775 - 2782. [Abstract] [Full Text] [PDF]
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D. Wang, Y. Chen, T. Chabrashvili, S. Aslam, L. J. Borrego Conde, J. G. Umans, and C. S. Wilcox Role of Oxidative Stress in Endothelial Dysfunction and Enhanced Responses to Angiotensin II of Afferent Arterioles from Rabbits Infused with Angiotensin II J. Am. Soc. Nephrol., November 1, 2003; 14(11): 2783 - 2789. [Abstract] [Full Text] [PDF]
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M.-S. Zhou, A. G. Adam, E. A. Jaimes, and L. Raij In Salt-Sensitive Hypertension, Increased Superoxide Production Is Linked to Functional Upregulation of Angiotensin II Hypertension, November 1, 2003; 42(5): 945 - 951. [Abstract] [Full Text] [PDF]
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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]
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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]
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Y. Wang, K. P. Patel, K. G. Cornish, K. M. Channon, and I. H. Zucker nNOS gene transfer to RVLM improves baroreflex function in rats with chronic heart failure Am J Physiol Heart Circ Physiol, October 1, 2003; 285(4): H1660 - H1667. [Abstract] [Full Text] [PDF]
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A. D. Dobrian, S. D. Schriver, T. Lynch, and R. L. Prewitt Effect of salt on hypertension and oxidative stress in a rat model of diet-induced obesity Am J Physiol Renal Physiol, October 1, 2003; 285(4): F619 - F628. [Abstract] [Full Text] [PDF]
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G. E. Callera, R. M. Touyz, S. A. Teixeira, M. N. Muscara, M. H. C. Carvalho, Z. B. Fortes, D. Nigro, E. L. Schiffrin, and R. C. Tostes ETA Receptor Blockade Decreases Vascular Superoxide Generation in DOCA-Salt Hypertension Hypertension, October 1, 2003; 42(4): 811 - 817. [Abstract] [Full Text] [PDF]
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K. K. Koh, J. Y. Ahn, S. H. Han, D. S. Kim, D. K. Jin, H. S. Kim, M.-S. Shin, T. H. Ahn, I. S. Choi, and E. K. Shin Pleiotropic effects of angiotensin II receptor blocker in hypertensive patients J. Am. Coll. Cardiol., September 3, 2003; 42(5): 905 - 910. [Abstract] [Full Text] [PDF]
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L. Li, S. W. Watts, A. K. Banes, J. J. Galligan, G. D. Fink, and A. F. Chen NADPH Oxidase-Derived Superoxide Augments Endothelin-1-Induced Venoconstriction in Mineralocorticoid Hypertension Hypertension, September 1, 2003; 42(3): 316 - 321. [Abstract] [Full Text] [PDF]
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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]
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S. P. Didion and F. M. Faraci Angiotensin II Produces Superoxide-Mediated Impairment of Endothelial Function in Cerebral Arterioles Stroke, August 1, 2003; 34(8): 2038 - 2042. [Abstract] [Full Text] [PDF]
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T. Chabrashvili, C. Kitiyakara, J. Blau, A. Karber, S. Aslam, W. J. Welch, and C. S. Wilcox Effects of ANG II type 1 and 2 receptors on oxidative stress, renal NADPH oxidase, and SOD expression Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2003; 285(1): R117 - R124. [Abstract] [Full Text] [PDF]
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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]
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J. Liu, F. Yang, X.-P. Yang, M. Jankowski, and P. J. Pagano NAD(P)H Oxidase Mediates Angiotensin II-Induced Vascular Macrophage Infiltration and Medial Hypertrophy Arterioscler Thromb Vasc Biol, May 1, 2003; 23(5): 776 - 782. [Abstract] [Full Text] [PDF]
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B. Yuan, M. Liang, Z. Yang, E. Rute, N. Taylor, M. Olivier, and A. W. Cowley Jr. Gene expression reveals vulnerability to oxidative stress and interstitial fibrosis of renal outer medulla to nonhypertensive elevations of ANG II Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2003; 284(5): R1219 - R1230. [Abstract] [Full Text] [PDF]
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