p22phox in the macula densa regulates single nephron GFR during angiotensin II infusion in rats

2007 ◽  
Vol 292 (4) ◽  
pp. H1685-H1689 ◽  
Author(s):  
Pouneh Nouri ◽  
Pritmohinder Gill ◽  
Min Li ◽  
Christopher S. Wilcox ◽  
William J. Welch
Keyword(s):  
Angiotensin Ii ◽  
Nadph Oxidase ◽  
Blood Pressure Response ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Distal Tubule ◽  
Macula Densa ◽  
Tubuloglomerular Feedback ◽  
Ang Ii ◽  
Renal Vasoconstriction ◽  
Single Nephron

Angiotensin II (ANG II) infusion increases renal superoxide (O2−) and enhances renal vasoconstriction via macula densa (MD) regulation of tubuloglomerular feedback, but the mechanism is unclear. We targeted the p22 phox subunit of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) with small-interfering RNA (siRNA) to reduce NADPH oxidase activity and blood pressure response to ANG II in rats. We compared single nephron glomerular filtration rate (SNGFR) in samples collected from the proximal tubule (PT), which interrupts delivery to the MD, and from the distal tubule (DT), which maintains delivery to the MD, to assess MD regulation of GFR. SNGFR was measured in control and ANG II-infused rats (200 ng·kg−1·min−1 for 7 days) 2 days after intravenous injection of vehicle or siRNA directed to p22 phox to test the hypothesis that p22 phox mediates MD regulation of SNGFR during ANG II. The regulation of SNGFR by MD, determined by PT SNGFR-DT SNGFR, was not altered by siRNA in control rats (control + vehicle, 13 ± 1, n = 8; control + siRNA, 12 ± 2 nl/min, n = 8; not significant) but was reduced by siRNA in ANG II-treated rats (ANG II + vehicle, 13 ± 2, n = 7; ANG II + siRNA, 7 ± 1 nl/min, n = 8; P < 0.05). We conclude that p22 phox and NADPH oxidase regulate the SNGFR during ANG II infusion via MD-dependent mechanisms.

scholarly journals NOX2 is the primary source of angiotensin II-induced superoxide in the macula densa

2010 ◽  
Vol 298 (3) ◽  
pp. R707-R712 ◽  
Author(s):  
Yiling Fu ◽  
Rui Zhang ◽  
Deyin Lu ◽  
Haifeng Liu ◽  
Kiran Chandrashekar ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Nadph Oxidase ◽  
Primary Source ◽  
Oxidase Inhibitor ◽  
Macula Densa ◽  
Tubuloglomerular Feedback ◽  
Ang Ii ◽  
Xanthine Oxidase Inhibitor ◽  
Si Rna ◽  
Full Activation

Macula densa (MD)-mediated regulation of renal hemodynamics via tubuloglomerular feedback is regulated by interactions between factors such as superoxide (O2−) and angiotensin II (ANG II). We have reported that NaCl-induced O2−in the MD is produced by the NOX2 isoform of NADPH oxidase (NOX); however, the source of ANG II-induced O2−in MD is unknown. Thus we determined the pathways by which ANG II increased O2−in the MD by measuring O2−in ANG II-treated MMDD1 cells, a MD-like cell line. ANG II caused MMDD1 O2−levels to increase by more than twofold ( P < 0.01). This increase was blocked by losartan (AT1receptor blocker) but not PD-123319 (AT2receptor antagonist). Apocynin (a NOX inhibitor) decreased O2−by 86% ( P < 0.01), whereas oxypurinol (a xanthine oxidase inhibitor) and NS-398 (a cyclooxygenase-2 inhibitor) had no significant effect. The NOX-dependent increase in O2−was due to the NOX2 isoform; a short interfering (si)RNA against NOX2 blunted ANG II-induced increases in O2−, whereas the NOX4/siRNA did not. Finally, we found that inhibiting the Rac1 subunit of NOX blunted ANG II-induced O2−production in NOX4/siRNA-treated cells but did not further decrease it in NOX2/siRNA-treated cells. Our results indicate that ANG II stimulates O2−production in the MD primarily via AT1-dependent activation of NOX2. Rac1 is required for the full activation of NOX2. This pathway may be an important component of ANG II enhancement of tubuloglomerular feedback.

Angiotensin-induced defects in renal oxygenation: role of oxidative stress

2005 ◽  
Vol 288 (1) ◽  
pp. H22-H28 ◽  
Author(s):  
William J. Welch ◽  
Jonathan Blau ◽  
Hui Xie ◽  
Tina Chabrashvili ◽  
Christopher S. Wilcox
Keyword(s):  
Angiotensin Ii ◽  
Nadph Oxidase ◽  
Glass Electrode ◽  
Ang Ii ◽  
Renal Vasoconstriction ◽  
Mrna And Protein Expression ◽  
Renal Vascular ◽  
Induced Defects ◽  
Renal Oxygen

We tested the hypothesis that superoxide anion (O2−·) generated in the kidney by prolonged angiotensin II (ANG II) reduces renal cortical Po2 and the use of O2 for tubular sodium transport (TNa:QO2). Groups ( n = 8–11) of rats received angiotensin II (ANG II, 200 ng·kg−1·min−1 sc) or vehicle for 2 wk with concurrent infusions of a permeant nitroxide SOD mimetic 4-hydroxy-2,2,6,6-tetramethylpiperidine 1-oxyl (Tempol, 200 nmol·kg−1·min−1) or vehicle. Rats were studied under anesthesia with measurements of renal oxygen usage and Po2 in the cortex and tubules with a glass electrode. Compared with vehicle, ANG II increased mean arterial pressure (107 ± 4 vs. 146 ± 6 mmHg; P < 0.001), renal vascular resistance (42 ± 3 vs. 65 ± 7 mmHg·ml−1·min−1·100 g−1; P < 0.001), renal cortical NADPH oxidase activity (2.3 ± 0.2 vs. 3.6 ± 0.4 nmol O2−··min−1·mg−1 protein; P < 0.05), mRNA and protein expression for p22 phox (2.1- and 1.8-fold respectively; P < 0.05) and reduced the mRNA for extracellular (EC)-SOD (−1.8 fold; P < 0.05). ANG II reduced the Po2 in the proximal tubule (39 ± 1 vs. 34 ± 2 mmHg; P < 0.05) and throughout the cortex and reduced the TNa:QO2 (17 ± 1 vs. 9 ± 2 μmol/μmol; P < 0.001). Tempol blunted or prevented all these effects of ANG II. The effects of prolonged ANG II to cause hypertension, renal vasoconstriction, renal cortical hypoxia, and reduced efficiency of O2 usage for Na+ transport, activation of NADPH oxidase, increased expression of p22 phox, and reduced expression of EC-SOD can be ascribed to O2−· generation because they are prevented by an SOD mimetic.

Tubuloglomerular feedback in ACE-deficient mice

1999 ◽  
Vol 276 (5) ◽  
pp. F751-F757 ◽  
Author(s):  
Timothy Traynor ◽  
Tianxin Yang ◽  
Yuning G. Huang ◽  
John H. Krege ◽  
Josie P. Briggs ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Response ◽  
Signal Transmission ◽  
Macula Densa ◽  
Mutant Mice ◽  
Tubuloglomerular Feedback ◽  
Ang Ii ◽  
Null Mutant ◽  
Nacl Concentration ◽  
Null Mutant Mice

In these experiments, we used a strain of angiotensin converting enzyme (ACE) germline null mutant mice, generated by J. H. Krege and co-workers (J. H. Krege, S. W. M. John, L. L. Langenbach, J. B. Hodgin, J. R. Hagaman, E. S. Bachman, J. C. Jennette, D. A. O’Brien, and O. Smithies. Nature 375: 146–148, 1995), to examine the effect of chronic ACE deficiency on the magnitude of tubuloglomerular feedback (TGF) responses. The genotype was determined by PCR on DNA extracted from the tail and was verified after each experiment by assessment of the blood pressure response to an injection of ANG I. To assess TGF responsiveness, we determined the change in stop-flow pressure (PSF) caused by increasing NaCl concentration at the macula densa by using micropuncture techniques. When loop of Henle flow rate was increased from 0 to 40 nl/min, PSF fell from a mean of 42.3 ± 1.95 to 33.6 ± 2.09 mmHg ( n = 6, P = 0.005) in wild-type mice (+/+), fell from 40.6 ± 2.35 to 38.6 ± 1.93 mmHg in heterozygous (+/−) mice ( n = 7, P = 0.014), and did not change in homozygous ACE (−/−) mice [36.7 ± 2.02 mmHg vs. 36.4 ± 2.01 mmHg; n = 4, P = not significant (NS)]. During an infusion of ANG II at a dose that did not significantly elevate blood pressure (70 ng ⋅ kg−1 ⋅ min−1), TGF response magnitude (PSF 0 − PSF 40) increased from 6.5 ± 1.4 to 9.8 ± 1.19 mmHg in +/+ ( P = 0.006), from 1.14 ± 0.42 to 4.6 ± 1.3 mmHg in +/− ( P = 0.016), and from 0.42 ± 0.25 to 4.02 ± 1.06 in −/− mice ( P = 0.05). Absence of TGF responses in ACE null mutant mice and restoration of near-normal responses during an acute infusion of ANG II supports previous conclusions that ANG II is an essential component in the signal transmission pathway that links the macula densa with the glomerular vascular pole.

scholarly journals Glomerular Hyperfiltration in Experimental Diabetes Mellitus

1999 ◽  
Vol 10 (12) ◽  
pp. 2569-2576
Author(s):  
VOLKER VALLON ◽  
KERSTIN RICHTER ◽  
ROLAND C. BLANTZ ◽  
SCOTT THOMSON ◽  
HARTMUT OSSWALD
Keyword(s):  
Diabetes Mellitus ◽  
Distal Tubule ◽  
Diabetic Rats ◽  
Macula Densa ◽  
Tubuloglomerular Feedback ◽  
Glomerular Hyperfiltration ◽  
Feedback Signal ◽  
Early Diabetes ◽  
Nondiabetic Control ◽  
Single Nephron

Abstract. An increase in Na+/glucose cotransport upstream to the macula densa might contribute to the increase in single nephron GFR (SNGFR) in early diabetes mellitus by lowering the signal of the tubuloglomerular feedback, i.e., the luminal Na+, Cl-, and K+ concentration sensed by the macula densa. To examine this issue, micropuncture experiments were performed in nephrons with superficial glomeruli of streptozotocin-induced diabetes mellitus in rats. First, in nondiabetic control rats, ambient early distal tubular concentrations of Na+, Cl-, and K+ were about 21, 20, and 1.2 mM, respectively, suggesting collection sites relatively close to the macula densa. Second, glomerular hyperfiltration in diabetic rats was associated with a reduction in ambient early distal tubular concentrations of Na+, Cl-, and K+ by 20 to 28%, reflecting an increase in fractional reabsorption of these ions up to the early distal tubule. Third, in diabetic rats, early proximal tubular application of phlorizin, an inhibitor of Na+/glucose cotransport, elicited (1) a greater reduction in absolute and fractional reabsorption of Na+, Cl-, and K+ up to the early distal tubule, and (2) a greater increase in early distal tubular concentration of these ions, which was associated with a more pronounced reduction in SNGFR. These findings support the concept that stimulation of tubular Na+/glucose cotransport by reducing the tubuloglomerular feedback signal at the macula densa may contribute to glomerular hyperfiltration in diabetic rats. Glomerular hyperfiltration in diabetic rats serves to compensate for the rise in fractional tubular reabsorption to partly restore the electrolyte load to the distal nephron.

Renal and tubuloglomerular feedback effects of [Sar1,Ala8]angiotensin II in the rat

1982 ◽  
Vol 242 (2) ◽  
pp. F149-F157 ◽  
Author(s):  
D. W. Ploth ◽  
R. N. Roy
Keyword(s):  
Angiotensin Ii ◽  
Proximal Tubule ◽  
Renin Angiotensin System ◽  
Distal Tubule ◽  
Plasma Renin ◽  
Tubuloglomerular Feedback ◽  
Ang Ii ◽  
Renin Angiotensin ◽  
Peritubular Capillaries ◽  
Angiotensin Blockade

Experiments were done in normal rats to assess kidney, single nephron, and tubuloglomerular feedback responses during control conditions and during renin-angiotensin blockade with the angiotensin II (ANG II) antagonist [Sar1,Ala8]angiotensin II (saralasin, 20 micrograms.kg-1.min-1). Plasma renin activity was increased fourfold during saralasin infusion. Glomerular filtration rate (GFR) and renal blood flow increased in parallel from 1.09 +/- 0.04 to 1.26 +/- 0.05 ml/min and from 6.4 +/- 0.5 to 7.6 +/- 0.5 ml/min, respectively. Absolute and fractional sodium excretion were increased sixfold during ANG II blockade. Hydrostatic pressures in proximal tubules, peritubular capillaries, and distal tubules were unchanged. Estimates of nephron GFR (SNGFR) based on collections of distal tubular fluid were increased from 21.6 +/- 1.2 to 24.3 +/- 0.9 nl/min during ANG II blockade. Increases in SNGFR and decreases in fractional absorption at micropuncture sites beyond the late proximal tubule during saralasin administration resulted in increases of flow rate and Cl- delivery at the early distal tubule. Tubuloglomerular feedback activity, assessed by measuring changes in proximal tubule stop-flow pressure in response to alterations in orthograde microperfusion rate from late proximal tubule sites, was significantly attenuated over the range of physiological flow rates for the late proximal tubule during blockade of the renin-angiotensin system. Acute blockade of ANG II in this rat model results in attenuated tubuloglomerular feedback activity and associated changes of hemodynamic and excretory behavior by the kidney.

Oxidative stress is a critical mediator of the angiotensin II signal in human neutrophils: involvement of mitogen-activated protein kinase, calcineurin, and the transcription factor NF-κB

Blood ◽  
2003 ◽  
Vol 102 (2) ◽  
pp. 662-671 ◽  
Author(s):  
Rajaa El Bekay ◽  
Moisés Álvarez ◽  
Javier Monteseirín ◽  
Gonzalo Álba ◽  
Pedro Chacón ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Angiotensin Ii ◽  
Nadph Oxidase ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Human Neutrophils ◽  
Published Data ◽  
Calcium Stores ◽  
Ang Ii ◽  
O2 Production

Abstract Neutrophils are mobilized to the vascular wall during vessel inflammation. Published data are conflicting on phagocytic nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase activation during the hypertensive state, and the capacity of angiotensin II (Ang II) to modulate the intracellular redox status has not been analyzed in neutrophils. We here describe that Ang II highly stimulates endogenous and extracellular O2- production in these cells, consistent with the translocation to the cell membrane of the cytosolic components of NADPH oxidase, p47phox, and p67phox. The Ang II–dependent O2- production was suppressed by specific inhibitors of AT1 receptors, of the p38MAPK and ERK1/2 pathways, and of flavin oxidases. Furthermore, Ang II induced a robust phosphorylation of p38MAPK, ERK1/2, and JNK1/2 (particularly JNK2), which was hindered by inhibitors of NADPH oxidase, tyrosine kinases, and ROS scavengers. Ang II increased cytosolic Ca2+ levels—released mainly from calcium stores—enhanced the synthesis de novo and activity of calcineurin, and stimulated the DNA-binding activity of the transcription factor NF-κB in cultured human neutrophils. Present data demonstrate for the first time a stimulatory role of Ang II in the activation of phagocytic cells, underscore the relevant role of ROS as mediators in this process, and uncover a variety of signaling pathways by which Ang II operates in human neutrophils.

Angiotensin II directly stimulates macula densa Na-2Cl-K cotransport via apical AT1 receptors

2002 ◽  
Vol 282 (2) ◽  
pp. F301-F306 ◽  
Author(s):  
Gergely Kovács ◽  
János Peti-Peterdi ◽  
László Rosivall ◽  
P. Darwin Bell
Keyword(s):  
Angiotensin Ii ◽  
Fluorescence Microscopy ◽  
Initial Rate ◽  
Macula Densa ◽  
Tubuloglomerular Feedback ◽  
Ang Ii ◽  
At1 Receptors ◽  
Twofold Increase ◽  
Nacl Concentration ◽  
Sodium Binding

ANG II is a modulator of tubuloglomerular feedback (TGF); however, the site of its action remains unknown. Macula densa (MD) cells sense changes in luminal NaCl concentration ([NaCl]L) via a Na-2Cl-K cotransporter, and these cells do possess ANG II receptors. We tested whether ANG II regulates Na-2Cl-K cotransport in MD cells. MD cell Na+ concentration ([Na+]i) was measured using sodium-binding benzofuran isophthalate with fluorescence microscopy. Resting [Na+]i in MD cells was 27.7 ± 1.05 mM ( n = 138) and increased (Δ[Na+]i) by 18.5 ± 1.14 mM ( n = 17) at an initial rate (Δ[Na+]i/Δ t) of 5.54 ± 0.53 × 10−4 U/s with an increase in [NaCl]L from 25 to 150 mM. Both Δ[Na+]i and Δ[Na+]i/Δ t were inhibited by 80% with 100 μM luminal furosemide. ANG II (10−9 or 10−12 M) added to the lumen increased MD resting [Na+]i and [NaCl]L-dependent Δ[Na+]i and caused a twofold increase in Δ[Na+]i/Δ t. Bath (10−9 M) ANG II also stimulated cotransport activity, and there was no additive effect of simultaneous addition of ANG II to bath and lumen. The effects of luminal ANG II were furosemide sensitive and abolished by the AT1 receptor blocker candesartan. ANG II at 10−6 M failed to stimulate the cotransporter, whereas increased cotransport activity could be restored by blocking AT2 receptors with PD-123, 319. Thus ANG II may modulate TGF responses via alterations in MD Na-2Cl-K cotransport activity.

scholarly journals A new mechanism for the sex differences in angiotensin II-induced hypertension: the role of macula densa NOS1β-mediated tubuloglomerular feedback

2020 ◽  
Vol 319 (5) ◽  
pp. F908-F919
Author(s):  
Jie Zhang ◽  
Larry Qu ◽  
Jin Wei ◽  
Shan Jiang ◽  
Lan Xu ◽  
...  
Keyword(s):  
Sex Differences ◽  
Angiotensin Ii ◽  
Knockout Mice ◽  
Macula Densa ◽  
Tubuloglomerular Feedback ◽  
Ang Ii ◽  
Wild Type ◽  
Induced Hypertension

Females are protected against the development of angiotensin II (ANG II)-induced hypertension compared with males, but the mechanisms have not been completely elucidated. In the present study, we hypothesized that the effect of ANG II on the macula densa nitric oxide (NO) synthase 1β (NOS1β)-mediated tubuloglomerular feedback (TGF) mechanism is different between males and females, thereby contributing to the sexual dimorphism of ANG II-induced hypertension. We used microperfusion, micropuncture, clearance of FITC-inulin, and radio telemetry to examine the sex differences in the changes of macula densa NOS1β expression and activity, TGF response, natriuresis, and blood pressure (BP) after a 2-wk ANG II infusion in wild-type and macula densa-specific NOS1 knockout mice. In wild-type mice, ANG II induced higher expression of macula densa NOS1β, greater NO generation by the macula densa, and a lower TGF response in vitro and in vivo in females than in males; the increases of glomerular filtration rate, urine flow rate, and Na+ excretion in response to an acute volume expansion were significantly greater and the BP responses to ANG II were significantly less in females than in males. In contrast, these sex differences in the effects of ANG II on TGF, natriuretic response, and BP were largely diminished in knockout mice. In addition, tissue culture of human kidney biopsies (renal cortex) with ANG II resulted in a greater increase in NOS1β expression in females than in males. In conclusion, macula densa NOS1β-mediated TGF is a novel and important mechanism for the sex differences in ANG II-induced hypertension.

scholarly journals Endothelin-1-Induced Microvascular ROS and Contractility in Angiotensin-II-Infused Mice Depend on COX and TP Receptors

Antioxidants ◽  
2019 ◽  
Vol 8 (6) ◽  
pp. 193 ◽  
Author(s):  
Christopher S. Wilcox ◽  
Cheng Wang ◽  
Dan Wang
Keyword(s):  
Angiotensin Ii ◽  
Nadph Oxidase ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Ros Generation ◽  
Oxygen Species ◽  
Ang Ii ◽  
Wild Type ◽  
Endothelin 1 ◽  
Ros Metabolism ◽  
Tp Receptors

(1) Background: Angiotensin II (Ang II) and endothelin 1 (ET-1) generate reactive oxygen species (ROS) that can activate cyclooxygenase (COX). However, thromboxane prostanoid receptors (TPRs) are required to increase systemic markers of ROS during Ang II infusion in mice. We hypothesized that COX and TPRs are upstream requirements for the generation of vascular ROS by ET-1. (2) Methods: ET-1-induced vascular contractions and ROS were assessed in mesenteric arterioles from wild type (+/+) and knockout (−/−) of COX1 or TPR mice infused with Ang II (400 ng/kg/min × 14 days) or a vehicle. (3) Results: Ang II infusion appeared to increase microvascular protein expression of endothelin type A receptors (ETARs), TPRs, and COX1 and 2 in COX1 and TPR +/+ mice but not in −/− mice. Ang II infusion increased ET-1-induced vascular contractions and ROS, which were prevented by a blockade of COX1 and 2 in TPR +/+ mice. ET-1 increased the activity of aortic nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and decreased superoxide dismutase (SOD) 1, 2, and 3 in Ang-II-infused mice, which were prevented by a blockade of TPRs. (4) Conclusion: Activation of vascular TPRs by COX products are required for ET-1 to increase vascular contractions and ROS generation from NADPH oxidase and reduce ROS metabolism by SOD. These effects require an increase in these systems by prior infusion of Ang II.

Reactive Oxygen Species-Mediated Homologous Downregulation of Angiotensin II Type 1 Receptor Mrna by Angiotensin II

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 688-688
Author(s):  
Toshihiro Ichiki ◽  
Kotaro Takeda ◽  
Akira Takeshita
Keyword(s):  
Reactive Oxygen Species ◽  
Angiotensin Ii ◽  
Nadph Oxidase ◽  
Mrna Expression ◽  
Crucial Role ◽  
Oxygen Species ◽  
Ang Ii ◽  
Stimulation Of

58 Recent studies suggest a crucial role of reactive oxygen species (ROS) for the signaling of Angiotensin II (Ang II) through type 1 Ang II receptor (AT1-R). However, the role of ROS in the regulation of AT1-R expression has not been explored. In this study, we examined the effect of an antioxidant on the homologous downregulation of AT1-R by Ang II. Ang II (10 -6 mol/L) decreased AT1-R mRNA with a peak suppression at 6 hours of stimulation in rat aortic vascular smooth muscle cells (VSMC). Ang II dose-dependently (10 -8 -10 -6 ) suppressed AT1-R mRNA at 6 hours of stimulation. Preincubation of VSMC with N-acetylcysteine (NAC), a potent antioxidant, almost completely inhibited the Ang II-induced downregulation of AT1-R mRNA. The effect of NAC was due to stabilization of the AT1-R mRNA that was destabilized by Ang II. Ang II did not affect the promoter activity of AT1-R gene. Diphenylene iodonium (DPI), an inhibitor of NADH/NADPH oxidase failed to inhibit the Ang II-induced AT1-R mRNA downregulation. The Ang II-induced AT1-R mRNA downregulation was also blocked by PD98059, an extracellular signal-regulated protein kinase (ERK) kinase inhibitor. Ang II-induced ERK activation was inhibited by NAC as well as PD98059 whereas DPI did not inhibit it. To confirm the role of ROS in the regulation of AT1-R mRNA expression, VSMC were stimulated with H 2 O 2 . H 2 O 2 suppressed the AT1-R mRNA expression and activated ERK. These results suggest that production of ROS and activation of ERK are critical for downregulation of AT1-R mRNA. The differential effect of NAC and DPI on the downregulation of AT1-R mRNA may suggest the presence of other sources than NADH/NADPH oxidase pathway for ROS in Ang II signaling. Generation of ROS through stimulation of AT1-R not only mediates signaling of Ang II but may play a crucial role in the adaptation process of AT1-R to the sustained stimulation of Ang II.

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