Effect of medial calcification on vascular function in uremia

Sutliff, Roy L.; Walp, Erik R.; El-Ali, Alexander; Elkhatib, Stacey; Lomashvili, Koba A.; O’Neill, W. Charles

doi:10.1152/ajprenal.00533.2010

Cited by 30 publications

(31 citation statements)

References 33 publications

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“…To our knowledge, arterial functions have been investigated in one previous study in animals with A-CRF although only the aorta was examined (29). In that study, concentrations of adenine (0.75%) and phosphate in the chow were higher than in the present study, and 0.22% NaCl was added to drinking water.…”

Section: Table 5 Responses To Ach In Mesenteric Arteries Preincubatecontrasting

confidence: 52%

Vascular function in rats with adenine-induced chronic renal failure

Nguy

Nilsson

Lundgren

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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G. Vascular function in rats with adenineinduced chronic renal failure. Am J Physiol Regul Integr Comp Physiol 302: R1426 -R1435, 2012. First published April 18, 2012 doi:10.1152/ajpregu.00696.2011The aim of the present study was to characterize the function of resistance arteries, and the aorta, in rats with adenine-induced chronic renal failure (A-CRF). Sprague-Dawley rats were randomized to chow with or without adenine supplementation. After 6 -10 wk, mesenteric arteries and thoracic aortas were analyzed ex vivo by wire myography. Plasma creatinine concentrations were elevated twofold at 2 wk, and eight-fold at the time of death in A-CRF animals. Ambulatory systolic and diastolic blood pressures measured by radiotelemetry were significantly elevated in A-CRF animals from week 3 and onward. At death, A-CRF animals had anemia, hyperphosphatemia, hyperparathyroidism, and elevated plasma levels of asymmetric dimethylarginine and oxidative stress markers. There were no significant differences between groups in the sensitivity, or maximal response, to ACh, sodium nitroprusside (SNP), norepinephrine, or phenylephrine in either mesenteric arteries or aortas. However, in A-CRF animals, the rate of aortic relaxation was significantly reduced following washout of KCl (both in intact and endothelium-denuded aorta) and in response to ACh and SNP. Also the rate of contraction in response to KCl was significantly reduced in A-CRF animals both in mesenteric arteries and aortas. The media of A-CRF aortas was thickened and showed focal areas of fragmented elastic lamellae and disorganized smooth muscle cells. No vascular calcifications could be detected. These results indicate that severe renal failure for a duration of less than 10 wk in this model primarily affects the aorta and mainly slows the rate of relaxation. chronic kidney disease; endothelial function; vascular smooth muscle cells; hypertension; mesenteric arteries; aorta PATIENTS WITH CHRONIC KIDNEY disease (CKD) are at increased risk of cardiovascular (CV) disease and in dialysis patients CV mortality rates are at least 10-to 20-fold higher than in the general population (5). The risk increases already when glomerular filtration rate (GFR) falls below 60 ml·min Ϫ1 ·1.73m Ϫ2(6) and a majority of CKD patients die from CV disease before developing end-stage renal disease (25). The pathophysiological mechanisms causing the increase in CV risk in CKD patients are in many cases associated with comorbidity, such as primary hypertension, diabetes mellitus, hypercholesterolemia, and established atherosclerotic disease (5, 26). However, the risk of CV death is markedly elevated also in children and young adults with CKD, although these patients often lack comorbidity (20). Also, the causes of CV death are different in CKD patients compared with in the general population with an excess of sudden cardiac deaths (5). Arterial abnormalities in patients with end-stage renal disease are typically characterized by increased stiffness and medial calcifications, which may develop i...

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Section: Table 5 Responses To Ach In Mesenteric Arteries Preincubatecontrasting

confidence: 52%

Vascular function in rats with adenine-induced chronic renal failure

Nguy

Nilsson

Lundgren

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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“…This event is the reason for local clot formation and ultimate organ infarction (25). In addition, vascular smooth muscle and endothelial function are altered in renal failure (26). An increased recirculation by a larger AV fistula may result in similar endothelial changes also in other organs at stress such as the heart, indicated by the data in the present study.…”

Section: Discussionsupporting

confidence: 69%

Fistula Diameter Correlates with Echocardiographic Characteristics in Stable Hemodialysis Patients

Hadimeri

Smedby

Fransson

et al. 2015

Nephrology @ Point of Care

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Aims and background Left ventricular hypertrophy (LVH) is a common finding in hemodialysis patients. The aim of the present study was to investigate if the diameter of the distal radiocephalic fistula could influence left ventricular variables in stable hemodialysis patients. Methods Nineteen patients were investigated. Measurements of the diameter of the arteriovenous (AV) fistula were performed in 4 different locations. The patients were investigated using M-mode recordings and measurements in the 2D image. Doppler ultrasound was also performed. Transonic measurements were performed after ultrasound investigation. Results Fistula mean and maximal diameter correlated with left ventricular characteristics. Fistula flow correlated neither with the left ventricular characteristics nor with fistula diameters. Conclusions The maximal diameter of the distal AV fistula seems to be a sensitive marker of LVH in stable hemodialysis patients.

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“…The method, it is thought that 2, 8-dihydroxyadenine produced from adenine via oxidization through xanthine dehydrogenase is precipitated in the kidney tubules as kidney stones 13,14) . It has been reported that adenine administration induces chronic tubulointerstitial injury, causing increased plasma creatinine and blood urea nitrogen (BUN) concentrations [15][16][17][18] .…”

Section: Discussionmentioning

confidence: 99%

“…Animal models of CKD have been previously reported, mostly using rats 12,[15][16][17][18] . The CKD mouse model employed in the current study was induced by feeding the mice a diet containing 0.25% adenine for four weeks, which resulted in increases in the plasma creatinine and BUN concentrations to approximately four and three times that seen in the control mice.…”

Section: Discussionmentioning

confidence: 99%

Reduction of NO-mediated Relaxing Effects in the Thoracic Aorta in an Experimental Chronic Kidney Disease Mouse Model

Mori-Kawabe

Yasuda

Ito

et al. 2015

JAT

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Aim: Chronic kidney disease (CKD) is known to frequently cause cardiovascular events. However, it is unclear how renal dysfunction affects the vascular response. We herein studied the effects of renal dysfunction on the aortic behavior in adenine-fed mice, investigating mechanisms underlying the occurrence of cardiovascular events in CKD patients. Methods: Biochemical analyses of the plasma creatinine, blood urea nitrogen (BUN) and glucose levels and measurements of the blood pressure were performed using C57BL/6 mice fed with and without an adenine-containing diet. The relaxing effects of acetylcholine (ACh) or sodium nitropurusside (SNP) and effects of NO synthase (NOS) inhibitors on the contractions induced by phenylephrine (PE) were measured in endothelium-intact aortas obtained from both mice. Results: The mice fed 0.25% adenine for four weeks showed greater plasma creatinine and BUN concentrations than the control mice, suggesting that adenine-fed mice are a useful CKD model. Furthermore, ACh relaxed the PE-stimulated, endothelium-intact aortas, the effect of which was less potent in the adenine-fed mice than in the control mice. In contrast, the degree of SNP-induced relaxation of the aortas was the same in the adenine-fed mice and control mice. The 1-adrenergic agonist, PE, induced more potent absolute tension of the endothelium-intact aortas in the CKD model mice than in the control mice, while the NOS inhibitors, N-nitro-L-arginine (LNA) and asymmetric dimethylarginine (ADMA) enhanced the contraction effects of PE in both mice. Conclusions: The findings of this study indicate that spontaneous and stimulated NO release from the endothelium is decreased in the CKD model mouse aorta. The NO-mediated correlation between renal and elastic arterial endothelial dysfunction is suggested to be a cause of cardiovascular events in patients with CKD. J Atheroscler Thromb, 2015; 22: 845-853.

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Effect of medial calcification on vascular function in uremia

Cited by 30 publications

References 33 publications

Vascular function in rats with adenine-induced chronic renal failure

Vascular function in rats with adenine-induced chronic renal failure

Fistula Diameter Correlates with Echocardiographic Characteristics in Stable Hemodialysis Patients

Reduction of NO-mediated Relaxing Effects in the Thoracic Aorta in an Experimental Chronic Kidney Disease Mouse Model

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