Experimentally induced metabolic acidosis in rabbits modulates the interaction of aortic glycosaminoglycan with plasma low-density lipoprotein—An interesting observation about the association of acidosis and atherosclerosis

Tovar, Ana; Pecly, Inah Maria Drummond; Rangel, Ednei P.; Melo-Filho, Nelson M.; Mourāo, Paulo A.S.; Leite, Maurilo

doi:10.1016/j.atherosclerosis.2006.06.011

Cited by 8 publications

(7 citation statements)

References 28 publications

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“…For the first time, Tavor et al . indicated an association between acidosis and atherosclerosis [16]. In the present study, we investigated the effect of metabolic acidosis on endothelial permeability as well as serum NO and lipid concentrations in normal and high-cholesterol fed animals.…”

Section: Discussionmentioning

confidence: 98%

“…Acidosis is associated with reduced synthesis of Apo A through enhanced DNA binding activity of a repressor of apolipoprotein A gene [19]. Furthermore, acidosis increases interaction of arterial glucosaminoglycan with plasma LDL [16]. …”

Section: Discussionmentioning

confidence: 99%

“…Metabolic acidosis was induced by adding 0.75% NH 4 Cl (Sigma) in drinking water ad libitum as previously described [16]. Body weight was measured during the experiment.…”

Section: Methodsmentioning

confidence: 99%

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Experimental research Effect of experimentally induced metabolic acidosis on aortic endothelial permeability and serum nitric oxide concentration in normal and high-cholesterol fed rabbits

Khazaei¹,

Nematbakhsh²

2012

aoms

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IntroductionMetabolic acidosis is present in end stage renal disease. There is a link between enhanced endothelial permeability and accelerated atherosclerosis. In this study, we investigated the effect of experimentally induced metabolic acidosis on aortic endothelial permeability and serum nitric oxide (NO) concentration in normal and high-cholesterol fed rabbits.Material and methodsTwenty-four male rabbits were divided into four groups: normal, hypercholesterolemic, acidemic, and hypercholesterolemic plus acidemic. Acidosis and hypercholesterolemia were induced by drinking water containing ammonium chloride (NH4Cl), and cholesterol-rich animal chow (1%), respectively. After 6 weeks, blood samples were taken and endothelial permeability was measured using the Evans blue dye injection method.ResultsHypercholesterolemic animals had higher aortic endothelial permeability compared with normal groups (16.18 ±0.91 µg EB/g tissue vs. 12.89 ±0.66 µg EB/g tissue, p < 0.05). Acidosis significantly increased endothelial permeability in the normal group (17.10 ±0.56 µg/g tissue vs. 12.89 ± 0.66 µg/g tissue; p < 0.05) but did not further increase endothelial permeability in hypercholesterolemic animals (16.18 ±0.91 µg EB/g tissue vs. 17.29 ±0.46 µg EB/g tissue; p > 0.05). Serum total cholesterol, low density lipoprotein (LDL) and NO concentrations in hypercholesterolemic animals were significantly higher than the normal group and acidosis could not change them either in the normal or in the high-cholesterol diet group.ConclusionsAlterations of serum lipids and NO are not the main mechanism for accelerated atherosclerosis during metabolic acidosis. Acidosis increases aortic endothelial permeability at least in a normal diet which may be a possible mechanism for progression of atherosclerosis processes in end-stage renal disease.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

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Experimental research Effect of experimentally induced metabolic acidosis on aortic endothelial permeability and serum nitric oxide concentration in normal and high-cholesterol fed rabbits

Khazaei¹,

Nematbakhsh²

2012

aoms

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“…However, a beneficial effect of treatment and prevention of metabolic acidosis on the risk factors of cardiovascular disease has not been consistently addressed. The relationship between acidosis and atherosclerosis was suggested by a previous study from our laboratory, in which rabbits submitted to acid diet showed more pronounced atherosclerotic lesions, with higher aortic subendothelial glycosaminoglycan-LDL interaction, when compared to rabbits with normal blood pH [25]. In fact, in 1993, Morgan and Leake [17 ]observed that LDL oxidation is enhanced in low pH, and additional in vitro studies suggested that acidosis in the microenvironment of the vessels could be related to the increase in LDL oxidation [26].…”

Section: Discussionmentioning

confidence: 99%

One-Year Conservative Care Using Sodium Bicarbonate Supplementation Is Associated with a Decrease in Electronegative LDL in Chronic Kidney Disease Patients: A Pilot Study

Rizzetto¹,

Mafra

Barra³

et al. 2017

Cardiorenal Med

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Background: Chronic kidney disease (CKD) patients develop metabolic acidosis when approaching stages 3 and 4, a period in which accelerated atherogenesis may ensue. Studies in vitro show that low pH may increase low-density lipoprotein (LDL) oxidation, suggesting a role for chronic metabolic acidosis in atherosclerosis. The present study attempted to evaluate the effects of conservative care using oral sodium bicarbonate (NaHCO₃) supplementation on the electronegative LDL [LDL(-)], a minimally oxidized LDL, plasma levels in CKD patients. Methods: Thirty-one CKD patients were followed by a multidisciplinary team during 15 months of care in which 1.0 mmol/kg/day oral NaHCO₃ supplementation was first given in the third month. Blood samples were collected 3 months before the initiation of oral NaHCO₃ supplementation (T1), at the time of the beginning of supplementation (T2), and thereafter, each 4 months (T3, T4 and T5) until month 15 of care. Blood parameters and LDL(-) were measured from these collections. Results: After 12 months of conservative care, creatinine clearance (MDRD) was kept stable, and serum bicarbonate (HCO₃^-) increased from 20.5 ± 2.9 to 22.6 ± 1.1 mM (p < 0.003). LDL(-) plasma levels declined from 4.5 ± 3.3 to 2.1 ± 0.9 U/L (p < 0.007) after reaching mean serum HCO₃^- levels of 22.6 ± 1.1 mM. Conclusions: Conservative care using oral NaHCO₃ supplementation was able to stabilize renal function and decrease serum levels of LDL(-), a modified proatherogenic lipoprotein, only when mean serum HCO₃^- levels approached 22 mM. This study constitutes evidence that alkali therapy, in addition to its beneficial effect on renal disease progression, might serve as a preventive strategy to attenuate atherogenesis in CKD patients.

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“…Monocytes/macrophages play an important role in all stages of atherosclerosis and contribute to local microenvironmental changes such as hypoxia [1], ischemia [2], and acidosis [3]. Recently, it has been suggested that acidic microenvironments have a considerable effect on immune cells and their function [4,5].…”

Section: Introductionmentioning

confidence: 99%

Simvastatin inhibits acidic extracellular pH-activated, outward rectifying chloride currents in RAW264.7 monocytic-macrophage and human peripheral monocytes

Shi

Wang

Liu

et al. 2009

International Immunopharmacology

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Experimentally induced metabolic acidosis in rabbits modulates the interaction of aortic glycosaminoglycan with plasma low-density lipoprotein—An interesting observation about the association of acidosis and atherosclerosis

Cited by 8 publications

References 28 publications

Experimental research Effect of experimentally induced metabolic acidosis on aortic endothelial permeability and serum nitric oxide concentration in normal and high-cholesterol fed rabbits

Experimental research Effect of experimentally induced metabolic acidosis on aortic endothelial permeability and serum nitric oxide concentration in normal and high-cholesterol fed rabbits

One-Year Conservative Care Using Sodium Bicarbonate Supplementation Is Associated with a Decrease in Electronegative LDL in Chronic Kidney Disease Patients: A Pilot Study

Simvastatin inhibits acidic extracellular pH-activated, outward rectifying chloride currents in RAW264.7 monocytic-macrophage and human peripheral monocytes

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