Angiotensin II Induces a Rapid and Transient Increase of Reactive Oxygen Species

Rodrı́guez-Puyol, Manuel; Griera-Merino, Mercedes; Pérez-Rivero, Gema; Díez-Marqués, María L.; Ruiz-Torres, María Piedad; Rodríguez‐Puyol, Diego

doi:10.1089/152308602762197407

Cited by 24 publications

(19 citation statements)

References 23 publications

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“…51 The transient elevation of F 2 -isoprostanes after Ang II has been described in cell culture and ex vivo and may suggest the induction of compensatory antioxidant mechanisms, such as increased expression of extracellular superoxide dismutase. 52,53 That Ang II and NE both increased concentrations of F 2 -isoprostanes concurs with the observations of Aizawa et al, 54 who reported that both Ang II and NE increased free plasma F 2 -isoprostanes in rats, but conflicts with data from other studies. 55 Nevertheless, the lack of effect of NE on PRA or aldosterone suggests that NE increased F 2 -isoprostanes independently of activation of the RAAS.…”

Section: Discussionsupporting

confidence: 77%

Angiotensin II Induces Interleukin-6 in Humans Through a Mineralocorticoid Receptor–Dependent Mechanism

Luther

Gainer²,

Murphey³

et al. 2006

Hypertension

143

109

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This study tested the hypothesis that angiotensin promotes oxidative stress and inflammation in humans via aldosterone and the mineralocorticoid receptor. We measured the effect of intravenous aldosterone (0.7 mug/kg per hour for 10 hours followed by 0.9 mug/kg per hour for 4 hours) and vehicle in a randomized, double-blind crossover study in 11 sodium-restricted normotensive subjects. Aldosterone increased interleukin (IL)-6 (from 4.7+/-4.9 to 9.4+/-7.1 pg/mL; F=4.94; P=0.04) but did not affect blood pressure, serum potassium, or high-sensitivity C-reactive protein. We next conducted a randomized, double-blind, placebo-controlled, crossover study to measure the effect of 3-hour infusion of angiotensin II (2 ng/kg per minute) and norepinephrine (30 ng/kg per minute) on separate days after 2 weeks of placebo or spironolactone (50 mg per day) in 14 salt-replete normotensive subjects. Angiotensin II increased blood pressure (increase in systolic pressure: 13.7+/-7.5 and 15.2+/-9.4 mm Hg during placebo and spironolactone, respectively; P<0.001 for angiotensin II) and decreased renal plasma flow (-202+/-73 and -167+/-112 mL/min/1.73 kg/m(2); P<0.001 for angiotensin II effect) similarly during placebo and spironolactone. Spironolactone enhanced the aldosterone response to angiotensin II (increase of 17.0+/-10.6 versus 9.0+/-5.7 ng/dL; P=0.002). Angiotensin II transiently increased free plasma F(2)-isoprostanes similarly during placebo and spironolactone. Angiotensin II increased serum IL-6 concentrations during placebo (from 1.8+/-1.1 to 2.4+/-1.4 pg/mL; F=4.5; P=0.04) but spironolactone prevented this effect (F=6.4; P=0.03 for spironolactone effect). Norepinephrine increased blood pressure and F(2)-isoprostanes but not aldosterone or IL-6. Aldosterone increases IL-6 in humans. These data suggest that angiotensin II induces IL-6 through a mineralocorticoid receptor-dependent mechanism in humans. In contrast, angiotensin II-induced oxidative stress, as measured by F(2)-isoprostanes, is mineralocorticoid receptor independent and may be pressor dependent.

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Section: Discussionsupporting

confidence: 77%

Angiotensin II Induces Interleukin-6 in Humans Through a Mineralocorticoid Receptor–Dependent Mechanism

Luther

Gainer²,

Murphey³

et al. 2006

Hypertension

143

109

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“…These observations indicate that O 2 Ϫ augments, or partly mediates, the responses to ANG II in SHR. The latter is supported by observations that ANG II stimulation led to increased lucigenin chemiluminescence, indicating elevated production of ROS in response to ANG II (37,45). In the study by Shastri et al (45), inhibition of the NO system, by either L-NAME or endothelial denudation, abolished the effect of tempol on the ANG II response.…”

Section: Discussionmentioning

confidence: 78%

NO-independent mechanism mediates tempol-induced renal vasodilation in SHR

Richelieu¹,

Sørensen²,

Holstein‐Rathlou³

et al. 2005

American Journal of Physiology-Renal Physiology

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. NO-independent mechanism mediates tempol-induced renal vasodilation in SHR. Am J Physiol Renal Physiol 289: F1227-F1234, 2005. First published July 20, 2005; doi:10.1152/ajprenal.00116.2005.-We investigated whether tempol, a superoxide dismutase mimetic, affected renal hemodynamics and arterial pressure in spontaneously hypertensive rats (SHR) and Sprague-Dawley (SD) rats. We also examined whether tempol affected exaggerated renal vasoconstrictor responses to ANG II in SHR. To test whether the effects of tempol were due to a restored NO system, we used the NOS inhibitor N w -nitro-L-arginine methyl ester (L-NAME). Renal blood flow (RBF) and mean arterial pressure (MAP) were measured in vivo by electromagnetic flowmetry and arterial catheterization in 10-to 12-wk-old anesthetized SHR and SD rats. Systolic arterial pressure (SAP) was measured in conscious rats using the tail cuff method. Tempol (1 mM) was given in the drinking water to SD (SD-T) and SHR (SHR-T) for 5-7 days for RBF measurements and for 15 days for SAP measurements. Age-matched SD (SD-C) and SHR (SHR-C) were used as controls. ANG II (1-4 ng) was administered as a bolus via a renal artery catheter. L-NAME was administered intravenously for 15-20 min. Renal vascular resistance (RVR) was elevated in SHR-C compared with SD-C. In SHR-T, baseline RVR was not different from SD-C and SD-T rats. Tempol had no effect on RVR in SD. L-NAME elevated RVR to the same extent in all four groups. Arterial pressure was not affected by tempol. The RVR responses to ANG II were higher in SHR-C than in the SD-C group. ANG II responses were not different between SHR-T and SD-T. Overall, tempol reduced the renovascular responses to ANG II in SHR. L-NAME elevated the effects of ANG II in SD-C rats but had no effect on the ANG II responses in the other groups. Thus L-NAME treatment did not influence tempol's effects on baseline RVR or ANG II responses. We conclude that in SHR, tempol has a significant renal vasodilator effect and that it normalizes the increased renovascular ANG II sensitivity. As the effects of L-NAME are not greater in SHR-T rats, it is not likely that the elevated renal resistance and ANG II sensitivity in SHR are due to reactive oxygen speciesinduced quenching of nitric oxide. angiotensin II; hypertension; nitric oxide; oxidative stress; renal hemodynamics; spontaneously hypertensive rats KIDNEY FUNCTION IS of central importance in the control of normal blood pressure and in the development of essential hypertension (35,36). Spontaneously hypertensive rats (SHR) have an elevated renal vascular tone compared with normotensive rats (7,14,24). Also, an augmented response to vasoconstrictors, among them ANG II, has been observed in the genetically hypertensive rats (8,14,15,26,50). Despite intensive research, the reason for this enhanced renal vascular tone and reactivity in hypertensive animals is still not resolved.Elevated oxidative stress and high levels of reactive oxygen species (ROS) have been suggested to play a role in the pathogenesis of hyperten...

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“…As HMC release a great amount of active metabolites [20], a rather non-specific approach was selected, in which some pharmacological antagonists, including receptor antagonists for AII, platelet-activating factor and thromboxane A 2 , as well as a hydrogen peroxide scavenger, were used. The blocking concentrations of these antagonists were selected according to concentrations previously shown to be effective [23,36,37]. As shown in the Results section, losartan was the most efficient antagonist among those partially explain the observed results.…”

Section: Discussionmentioning

confidence: 96%

Crosstalk Between Mesangial and Endothelial Cells: Angiotensin II Down-Regulates Endothelin-Converting Enzyme 1

López‐Ongil¹,

Díez-Marqués

Griera

et al. 2005

Cell Physiol Biochem

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Objective: Since mesangial and endothelial cells interact in the kidney, the present experiments were designed to analyze the ability of human mesangial cells (HMC) to modulate endothelin-1 (ET-1) synthesis by human umbilical vein endothelial cells (HuVEC). Methods and Results: The supernatants of HuVEC/HMC contained significantly lower amounts of ET-1 than those of HuVEC alone. This effect was not due to a decreased prepro-ET-1 mRNA expression and was only partially the consequence of HMC-dependent ET-1 degradation. Therefore, we tested the influence of the coculture on endothelin-converting enzyme-1 (ECE-1), and found a significant reduction of its mRNA and protein levels as well as a decreased activity in HuVEC/HMC as compared to HuVEC alone. Using a pharmacological blockade approach (sulotrobam, BN52021, losartan or catalase), losartan was shown to completely abolish down-regulation of ECE-1 observed in HuVEC/HMC. Angiotensin II (AII) induced a dose and time-dependent inhibition of ECE-1 expression in HuVEC. Conclusions: These results support the importance of cross-talk among different cell types in the regulation of vascular or renal function. ET-1, and particularly ECE-1, might constitute a target in this regulation. In addition, locally synthesized AII could be one of the mediators involved in the down-regulation of ECE-1.

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Angiotensin II Induces a Rapid and Transient Increase of Reactive Oxygen Species

Cited by 24 publications

References 23 publications

Angiotensin II Induces Interleukin-6 in Humans Through a Mineralocorticoid Receptor–Dependent Mechanism

Angiotensin II Induces Interleukin-6 in Humans Through a Mineralocorticoid Receptor–Dependent Mechanism

NO-independent mechanism mediates tempol-induced renal vasodilation in SHR

Crosstalk Between Mesangial and Endothelial Cells: Angiotensin II Down-Regulates Endothelin-Converting Enzyme 1

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