scholarly journals High-fructose feeding impacts on the adrenergic control of renal haemodynamics in the rat

2011 ◽  
Vol 107 (2) ◽  
pp. 218-228 ◽  
Author(s):  
Mohammed H. Abdulla ◽  
Munavvar A. Sattar ◽  
Edward J. Johns ◽  
Nor A. Abdullah ◽  
Md. Abdul Hye Khan ◽  
...  
Keyword(s):  
Tap Water ◽  
High Dose ◽  
Ang Ii ◽  
Adrenergic Agonists ◽  
Sprague Dawley ◽  
Water Control ◽  
Renal Vasculature ◽  
Renal Vasoconstriction ◽  
Fructose Intake ◽  
High Fructose

The present study explored the hypothesis that a prolonged 8 weeks exposure to a high fructose intake suppresses adrenergic and angiotensin II (Ang II)-mediated vasoconstriction and is associated with a higher contribution of α1D-adrenoceptors. A total of thirty-two Sprague–Dawley rats received either 20 % fructose solution (FFR) or tap water (control, C) to drink ad libitum for 8 weeks. Metabolic and haemodynamic parameters were assessed weekly. The renal cortical vasoconstrictor responses to noradrenaline (NA), phenylephrine (PE), methoxamine (ME) and Ang II were determined in the presence and absence of BMY7378 (α1D-adrenoceptor antagonist). FFR had increased blood pressure, plasma levels of glucose, TAG and insulin. FFR expressed reduced renal vascular responses to adrenergic agonists and Ang II (NA: 50 %, PE: 50 %, ME, 65 %, Ang II: 54 %). Furthermore in the C group, the magnitude of the renal cortical vasoconstriction to all agonists was blunted in the presence of the low or high dose of BMY7378 (NA: 30 and 31 %, PE: 23 and 33 %, ME: 19 and 44 %, Ang II: 53 and 77 %), respectively, while in the FFR, vasoconstriction was enhanced to adrenergic agonists and reduced to Ang II (NA: 8 and 83 %, PE: 55 %, ME, 2 and 177 %, Ang II: 61 and 31 %). Chronic high fructose intake blunts vascular sensitivity to adrenergic agonists and Ang II. Moreover, blocking of the α1D-adrenoceptor subtype results in enhancement of renal vasoconstriction to adrenergic agonists, suggesting an inhibitory action of α1D-adrenoceptors in the FFR. α1D-Adrenoceptors buffer the AT1-receptor response in the renal vasculature of normal rats and fructose feeding suppressed this interaction.

Angiotensin II-mediated biphasic regulation of proximal tubular Na+/H+ exchanger 3 is impaired during oxidative stress

2011 ◽  
Vol 301 (2) ◽  
pp. F364-F370 ◽  
Author(s):  
Anees Ahmad Banday ◽  
Mustafa F. Lokhandwala
Keyword(s):  
Oxidative Stress ◽  
Protein Kinase ◽  
Tap Water ◽  
Buthionine Sulfoximine ◽  
Inhibitory Effect ◽  
Ang Ii ◽  
Sprague Dawley ◽  
High Concentration ◽  
Nitric Oxide Signaling ◽  
Proximal Tubular

Angiotensin (ANG) II via AT1 receptors (AT1Rs) maintains sodium homeostasis by regulating renal sodium transporters including Na+/H+ exchanger 3 (NHE3) in a biphasic manner. Low-ANG II concentration stimulates whereas high concentrations inhibit NHE3 activity. Oxidative stress has been shown to upregulate AT1R function that could modulate the ANG II-mediated NHE3 regulation. This study was designed to identify the signaling pathways responsible for ANG II-mediated biphasic regulation of proximal tubular NHE3 and the effect of oxidative stress on this phenomenon. Male Sprague-Dawley rats were chronically treated with a pro-oxidant l-buthionine sulfoximine (BSO) with and without an antioxidant tempol in tap water for 3 wk. BSO-treated rats exhibited oxidative stress and high blood pressure. At low concentration (1 pM) ANG II increased NHE3 activity in proximal tubules from all animals. However, in BSO-treated rats, the stimulation was more robust and was normalized by tempol treatment. ANG II (1 pM)-mediated NHE3 activation was abolished by AT1R blocker, intracellular Ca2+ chelator, and inhibitors of phospholipase C (PLC) and Ca2+-dependent calmodulin (CaM) but it was insensitive to Giα and protein kinase C inhibitors or AT2R antagonist. A high concentration of ANG II (1 μM) inhibited NHE3 activity in control and tempol-treated rats. However, in BSO-treated rats, ANG II (1 μM) continued to induce NHE3 stimulation. Tempol restored the inhibitory effect of ANG II (1 μM) in BSO-treated rats. The inhibitory effect of ANG II (1 μM) involved AT1R-dependent, cGMP-dependent protein kinase (PKG) activation and was independent of AT2 receptor and nitric oxide signaling. We conclude that ANG II stimulates NHE3 via AT1R-PLC-CaM pathway and inhibits NHE3 by AT1R-PKG activation. Oxidative stress impaired ANG II-mediated NHE3 biphasic response in that stimulation was observed at both high- and low-ANG II concentration.

Abstract 41: Fructose Stimulates Na/H Exchanger 3 Activity and Enhances the Ability of Angiotensin II to Activate Na/H Exchanger 3 in the Proximal Tubule

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Pablo Cabral ◽  
Nancy Hong ◽  
Jeffrey Garvin
Keyword(s):  
Angiotensin Ii ◽  
Proximal Tubule ◽  
Physiological Saline ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Basal Rate ◽  
Low Concentrations ◽  
Sprague Dawley Rats ◽  
High Fructose ◽  
Salt Sensitive Hypertension

Consumption of high-fructose corn syrup as a sweetener has increased dramatically. Fructose has been implicated in the epidemic of diabetes, obesity and hypertension including salt-sensitive hypertension. However, the mechanisms are poorly understood. The proximal nephron reabsorbs 60-70% of the fluid and Na, and most of the filtered bicarbonate via Na/H exchanger 3. Enhanced proximal nephron transport has been implicated in several forms of hypertension. We hypothesized that fructose stimulates NHE3 activity and enhances the ability of angiotensin II (ANG II) to activate NHE3 in the proximal tubule. To test our hypothesis we isolated and perfused proximal tubules from Sprague Dawley rats. NHE3 activity was measured as the recovery of intracellular pH after an NH4Cl acid pulse using the pH sensitive dye BCECF. The rate of pH recovery was measured in Fluorescent Units per second (FU/sec). In the presence of a 5.5 mM glucose-containing physiological saline the basal rate of pH recovery was 3.1 ± 0.8 FU/sec. When the luminal solution was exchanged to a 0.6 mM glucose + 5 mM fructose-containing physiological saline in a second period, the rate of pH recovery increased to 5 ± 1 FU/sec (p<0.03, n=8).To study whether this effect was due to the addition of fructose or the removal of glucose to the lumen, we performed a separate set of experiments where 5 mM glucose was substituted for 5 mM fructose. In the presence of 0.6 mM glucose the basal rate of pH recovery was 3.6 ± 1.5 FU/sec. When 5 mM fructose was added the rate of pH recovery increased to 5.9 ± 2 FU/sec (p<0.02, n=5). Control experiments showed no differences between periods when 5 mm glucose was added back to the luminal perfusate. Finally, we tested the effect of low concentrations of ANG II in the presence or absence of luminal fructose. In the presence of 5.5 mM glucose, ANG II 10-12 M did not affect the rate of pH recovery (change: -1.1 ± 0.5 FU/sec, n=9). However, in the presence of 5 mM fructose, ANG II increased the rate of pH recovery (change: 4.0 ± 2.2 FU/sec, p< 0.03 n=6). We conclude that acute treatment with fructose stimulates NHE3 activity and enhances the ability of ANG II to activate NHE3 in the proximal tubule. These results may partially explain the mechanism by which a fructose diet induces hypertension.

Effects of chloride channel blockers on rat renal vascular responses to angiotensin II and norepinephrine

2004 ◽  
Vol 286 (2) ◽  
pp. F323-F330 ◽  
Author(s):  
Joen Steendahl ◽  
Niels-Henrik Holstein-Rathlou ◽  
Charlotte Mehlin Sorensen ◽  
Max Salomonsson
Keyword(s):  
Angiotensin Ii ◽  
Niflumic Acid ◽  
Channel Blockers ◽  
Ang Ii ◽  
Renal Vasculature ◽  
Renal Vasoconstriction ◽  
Electromagnetic Flowmetry ◽  
Control Response ◽  
Renal Vascular

The aim of the present study was to investigate the role of Ca2+-activated Cl- channels in the renal vasoconstriction elicited by angiotensin II (ANG II) and norepinephrine (NE). Renal blood flow (RBF) was measured in vivo using electromagnetic flowmetry. Ratiometric photometry of fura 2 fluorescence was used to estimate intracellular free Ca2+ concentration ([Ca2+]i) in isolated preglomerular vessels from rat kidneys. Renal arterial injection of ANG II (2-4 ng) and NE (20-40 ng) produced a transient decrease in RBF. Administration of ANG II (10-7 M) and NE (5 × 10-6 M) to the isolated preglomerular vessels caused a prompt increase in [Ca2+]i. Renal preinfusion of DIDS (0.6 and 1.25 μmol/min) attenuated the ANG II-induced vasoconstriction to ∼35% of the control response, whereas the effects of NE were unaltered. Niflumic acid (0.14 and 0.28 μmol/min) and 2-[(2-cyclopentenyl-6,7-dichloro-2,3-dihydro-2-methyl-1-oxo-1 H-inden-5-yl)oxy]acetic acid (IAA-94; 0.045 and 0.09 μmol/min) did not affect the vasoconstrictive responses of these compounds. Pretreatment with niflumic acid (50 μM) or IAA-94 (30 μM) for 2 min decreased baseline [Ca2+]i but did not change the magnitude of the [Ca2+]i response to ANG II and NE in the isolated vessels. The present results do not support the hypothesis that Ca2+-activated Cl- channels play a crucial role in the hemodynamic effects of ANG II and NE in rat renal vasculature.

scholarly journals High-Dose Estradiol-Replacement Therapy Enhances the Renal Vascular Response to Angiotensin II via an AT2-Receptor Dependent Mechanism

2015 ◽  
Vol 2015 ◽  
pp. 1-7
Author(s):  
Tahereh Safari ◽  
Mehdi Nematbakhsh ◽  
Roger G. Evans ◽  
Kate M. Denton
Keyword(s):  
Angiotensin Ii ◽  
Replacement Therapy ◽  
Hormone Replacement ◽  
Renal Perfusion ◽  
Ovariectomized Rats ◽  
High Dose ◽  
Ang Ii ◽  
Renal Vasoconstriction ◽  
Increased Risk ◽  
Angiotensin Type 2 Receptor

Physiological levels of estrogen appear to enhance angiotensin type 2 receptor- (AT2R-) mediated vasodilatation. However, the effects of supraphysiological levels of estrogen, analogous to those achieved with high-dose estrogen replacement therapy in postmenopausal women, remain unknown. Therefore, we pretreated ovariectomized rats with a relatively high dose of estrogen (0.5 mg/kg/week) for two weeks. Subsequently, renal hemodynamic responses to intravenous angiotensin II (Ang II, 30–300 ng/kg/min) were tested under anesthesia, while renal perfusion pressure was held constant. The role of AT2R was examined by pretreating groups of rats with PD123319 or its vehicle. Renal blood flow (RBF) decreased in a dose-related manner in response to Ang II. Responses to Ang II were enhanced by pretreatment with estradiol. For example, at 300 ng kg−1 min−1, Ang II reduced RBF by45.7±1.9% in estradiol-treated rats but only by27.3±5.1% in vehicle-treated rats. Pretreatment with PD123319 blunted the response of RBF to Ang II in estradiol-treated rats, so that reductions in RBF were similar to those in rats not treated with estradiol. We conclude that supraphysiological levels of estrogen promote AT2R-mediated renal vasoconstriction. This mechanism could potentially contribute to the increased risk of cardiovascular disease associated with hormone replacement therapy using high-dose estrogen.

scholarly journals ADP-ribosyl cyclase and ryanodine receptors mediate endothelin ETA and ETB receptor-induced renal vasoconstriction in vivo

2008 ◽  
Vol 295 (2) ◽  
pp. F360-F368 ◽  
Author(s):  
Tiffany L. Thai ◽  
William J. Arendshorst
Keyword(s):  
Ryanodine Receptors ◽  
Ruthenium Red ◽  
Sprague Dawley ◽  
Renal Vasculature ◽  
Receptor Stimulation ◽  
Renal Vasoconstriction ◽  
Adp Ribosyl Cyclase ◽  
Etb Receptor ◽  
Rats And Mice

ADP-ribosyl cyclase (ADPR cyclase) and ryanodine receptors (RyR) participate in calcium transduction in isolated afferent arterioles. We hypothesized that this signaling pathway is activated by ETA and ETB receptors in the renal vasculature to mediate vasoconstriction in vivo. To test this, we measured acute renal blood flow (RBF) responses to ET-1 in anesthetized rats and mice in the presence and absence of functional ADPR cyclase and/or RyR. Inhibitors of ADPR cyclase (nicotinamide) or RyR (ruthenium red) reduced RBF responses to ET-1 by 44% ( P < 0.04 for both) in Sprague-Dawley rats. Mice lacking the predominant form of ADPR cyclase (CD38−/−) had RBF responses to ET-1 that were 47% weaker than those seen in wild-type mice ( P = 0.01). Selective ETA receptor stimulation (ET-1+BQ788) produced decreases in RBF that were attenuated by 43 and 56% by nicotinamide or ruthenium red, respectively ( P < 0.02 for both). ADPR cyclase or RyR inhibition also reduced vasoconstrictor effects of the ETB receptor agonist sarafotoxin 6c (S6c; 77 and 54%, respectively, P < 0.02 for both). ETB receptor stimulation by ET-1 + the ETA receptor antagonist BQ123 elicited responses that were attenuated by 59 and 60% by nicotinamide and ruthenium red, respectively ( P < 0.01 for both). Nicotinamide attenuated RBF responses to S6c by 54% during inhibition of nitric oxide synthesis ( P = 0.001). We conclude that in the renal microcirculation in vivo 1) ET-1-induced vasoconstriction is mediated by ADPR cyclase and RyR; 2) both ETA and ETB receptors activate this pathway; and 3) ADPR cyclase participates in ETB receptor signaling independently of NO.

Arterial lesions in dopamine-infused rats

1984 ◽  
Vol 42 ◽  
pp. 198-199
Author(s):  
P. J. Bugelski ◽  
C. Walsh Vockley ◽  
J. Sowinski ◽  
E. Arena ◽  
D. G. Morgan
Keyword(s):  
Intravenous Infusion ◽  
Adrenergic Receptors ◽  
Agonist Activity ◽  
Adrenergic Agonists ◽  
Sprague Dawley ◽  
Renal Vasculature ◽  
En Bloc ◽  
Sprague Dawley Rats ◽  
Arterial Lesions ◽  
Medial Necrosis

Dopamine is administered by intravenous infusion to maintain renal blood flow in patients with shock and congestive heart failure. This effect is probably due to dopamine receptors present in the renal vasculature. Dopamine also has agonist activity at α-adrenergic receptors which can evoke vasoconstriction. Alpha-adrenergic agonists produce medial necrosis in various arterial beds of the rat, including those in which dopamine exerts a vasodilator effect. To determine the effects on these arteries, we administered dopamine to rats by intravenous infusion and examined their gastric and renal arteries by transmission and scanning electron microscopy. Sprague Dawley rats were infused via tail vein with 20 μg/kg/min of dopamine HCl. For transmission EM (TEM), rats infused with dopamine for 1, 4 or 24 hours were perfused with 1% phosphate-buffered glutaraldehyde, post-fixed in 1% OsO4, stained en bloc with uranyl magnesium acetate, dehydrated and embedded in epoxy.

Effects of ANG II, ETA, and TxA2 receptor antagonists on cyclosporin A renal vasoconstriction

1994 ◽  
Vol 267 (3) ◽  
pp. F443-F449 ◽  
Author(s):  
J. D. Conger ◽  
G. E. Kim ◽  
J. B. Robinette
Keyword(s):  
Cyclosporin A ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Receptor Antagonists ◽  
Renal Vasoconstriction ◽  
Sprague Dawley Rats ◽  
Nonspecific Effects ◽  
Oxide Synthase ◽  
Renal Vascular

The renin-angiotensin system, endothelin (ET), and vasoconstrictor prostaglandins have been reported in separate studies to mediate the renal vasoconstrictor effect of cyclosporin A (CsA). However, direct comparison of the relative importance of these potential mediators has not been performed. In this study, the attenuating effects of comparable agonist-inhibiting doses of receptor antagonists for angiotensin II (ANG II), DuP-753 at 2.5 mg/kg, for ETA, BQ-123 at 0.5 mg/kg, and for thromboxane A2 (TxA2), SQ-29,548 at 1.6 mg.kg-1.h-1, or saline vehicle on acute CsA (20 mg/kg) renal vasoconstriction were compared in anesthetized Sprague-Dawley rats. All three receptor antagonists significantly limited the CsA-induced increase in renal vascular resistance; however, BQ-123 and SQ-29,548 were more effective than DuP-753. Because all three receptor antagonists demonstrated at least some attenuation of CsA-induced renal vasoconstriction, the potential role of acute CsA-related nitric oxide synthase (NOS) inhibition and nonspecific heterologous effects of specific receptor antagonists on other agonists were determined to exclude the possibilities that there was a general increased agonist sensitivity and that detection of a single or primary constrictor mediator was obscured by "crossover" receptor antagonist effects. CsA significantly reduced renal blood flow (39%) in the presence of the NOS inhibitor, N omega-nitro-L-arginine methyl ester, and there was negligible indication that receptor antagonists had nonspecific effects. It is concluded that CsA-induced renal vasoconstriction is complex and involves activation of multiple constrictor agonists independently or sequentially.

Effects of tempol on altered metabolism and renal vascular responsiveness in fructose-fed rats

2016 ◽  
Vol 41 (2) ◽  
pp. 210-218 ◽  
Author(s):  
Mohammed H. Abdulla ◽  
Munavvar A. Sattar ◽  
Edward J. Johns
Keyword(s):  
Drinking Water ◽  
Ang Ii ◽  
Adrenergic Agonists ◽  
Sprague Dawley ◽  
Insulin Resistant ◽  
Sprague Dawley Rats ◽  
Vascular Responsiveness ◽  
Altered Metabolism ◽  
Renal Vascular ◽  
Renal Responses

This study investigated the effect of tempol (a superoxide dismutase mimetic) on renal vasoconstrictor responses to angiotensin II (Ang II) and adrenergic agonists in fructose-fed Sprague–Dawley rats (a model of metabolic syndrome). Rats were fed 20% fructose in drinking water (F) for 8 weeks. One fructose-fed group received tempol (FT) at 1 mmol·L–1 in drinking water for 8 weeks or as an infusion (1.5 mg·kg–1·min–1) intrarenally. At the end of the treatment regimen, the renal responses to noradrenaline, phenylephrine, methoxamine, and Ang II were determined. F rats exhibited hyperinsulinemia, hyperuricemia, hypertriglyceridemia, and hypertension. Tempol reduced blood glucose and insulin levels (all p < 0.05) in FT rats compared with their untreated counterparts. The vasoconstriction response to all agonists was lower in F rats than in control rats by about 35%–65% (all p < 0.05). Vasoconstrictor responses to noradrenaline, phenylephrine, and methoxamine but not Ang II were about 41%–75% higher in FT rats compared with F rats (all p < 0.05). Acute tempol infusion blunted responses to noradrenaline, methoxamine, and Ang II in control rats by 32%, 33%, and 62%, while it blunted responses to noradrenaline and Ang II in F rats by 26% and 32%, respectively (all p < 0.05), compared with their untreated counterparts. Superoxide radicals play a crucial role in controlling renal vascular responses to adrenergic agonists in insulin-resistant rats. Chronic but not acute tempol treatment enhances renal vascular responsiveness in fructose-fed rats.

scholarly journals Serelaxin reduces oxidative stress and asymmetric dimethylarginine in angiotensin II-induced hypertension

2014 ◽  
Vol 307 (12) ◽  
pp. F1355-F1362 ◽  
Author(s):  
Jennifer M. Sasser ◽  
Mark W. Cunningham ◽  
Chris Baylis
Keyword(s):  
Oxidative Stress ◽  
Asymmetric Dimethylarginine ◽  
Oxidation Products ◽  
No Oxidation ◽  
Kidney Cortex ◽  
High Dose ◽  
Protective Effects ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Induced Hypertension

Recent findings suggest the therapeutic action of relaxin during hypertension is dependent on nitric oxide synthase (NOS) activation; however, the mechanisms underlying the beneficial effects of relaxin on the NOS system have not been fully elucidated. We hypothesized that the protective effects of relaxin include reducing both oxidative stress and the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA). We examined the effect of Serelaxin [human recombinant relaxin-2 (RLX)] in male Sprague-Dawley rats given high-dose angiotensin (ANG) II (400 ng·kg−1·min−1 sc) for 6 wk or shams. RLX was administered (4 μg/h sc) to half of the rats in each group after 2 wk of ANG II for the remaining 4 wk. ANG II induced hypertension and proteinuria, reduced NO oxidation products (NOx), and increased oxidative stress (NADPH oxidase activity, thiobarbituric acid-reactive substances, and 8-isoprostane excretion) and plasma ADMA. While RLX had no effect on sham rats, RLX attenuated the ANG II-dependent hypertension (165 ± 5 vs. 135 ± 13 mmHg, P < 0.05) and proteinuria at 6 wk (62 ± 6 vs. 41 ± 4 mg·day−1·100 g−1, P < 0.05) and normalized oxidative stress and circulating ADMA, in association with restored NOx excretion and kidney cortex NOx. We found that RLX had no impact on the ADMA-regulatory enzymes protein arginine methyltransferase and dimethylarginine-dimethylaminohydrolase (DDAH). Furthermore, RLX treatment did not increase DDAH activity in kidney cortex or liver. These data suggest that benefits of RLX treatment include reduced ADMA levels and increased NO bioavailability, possibly due to its antioxidant effects.

α2-Adrenergic mediation of the effects of angiotensin II on rat renal artery in vitro

1994 ◽  
Vol 72 (9) ◽  
pp. 1019-1024 ◽  
Author(s):  
David O. Ajikobi ◽  
William A. Cupples
Keyword(s):  
Angiotensin Ii ◽  
Renal Artery ◽  
Interactive Effects ◽  
Separate Experiment ◽  
Major Influence ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Renal Vasculature ◽  
Strong Concentration

Angiotensin II (ANG II) is a major influence on renal blood flow, acting directly on the renal vasculature and upon other controllers. In vivo observations suggest that ANG II affects renal artery resistance, although explicit in vitro studies have produced negative results. To resolve this issue, potential interactive effects of ANG II on renal artery in vitro were tested. Renal arteries were harvested from ketamine-anesthetized Sprague–Dawley rats and perfused in vitro at constant flow. Resistance was determined from the axial pressure drop while downstream pressure was held constant at ≈80 mmHg (1 mmHg = 133.3 Pa). ANG II, per se, had only a trivial effect on arterial diameter (−5.5 ± 1.5% at 10−7 M ANG II) and failed to affect resistance at concentrations ranging from 10−11 to 10−7 M. Norepinephrine caused strong concentration-dependent constriction, increasing resistance from 0.32 ± 0.04 to 1.86 ± 0.73 mmHg∙mL−1∙min at 10−6 M and 3.27 ± 0.88 mmHg∙mL−1∙min at 10−5 M. In the presence of 10−8 M ANG II, these responses were significantly increased to 3.31 ± 1.00 and 5.02 ± 1.22 mmHg∙mL−1∙min, respectively. Similarly, in the presence of 10−6 M norepinephrine, ANG II caused significant, concentration-dependent constriction of renal artery. In a separate experiment, 10−7 M yohimbine, a relatively specific antagonist of α2-adrenergic receptors, reversed the resistance increment due to ANG II, but not that due to norepinephrine. When yohimbine was applied before norepinephrine and ANG II, it did not affect the response to norepinephrine, but again blocked potentiation of the response by ANG II. The results indicate that, as occurs in some other vascular beds, ANG II "uncovers" vascular constriction that is mediated by α2-adrenergic receptors.Key words: vascular, resistance, interaction, norepinephrine, yohimbine.

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