Oxidative stress in patients with cardiovascular disease and chronic renal failure

Popolo, Ada; Autore, Giuseppina; Pinto, Aldo; Marzocco, Stefania

doi:10.3109/10715762.2013.779373

Cited by 145 publications

(100 citation statements)

References 100 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…There are indeed studies indicating that, under several pathological conditions, certain mechanisms that compensate deficient NO production may be activated [25,28,45]. In particular, these mechanisms include plasma oxidative stress, a condition existing in uremia [46,47], which can cause a paradoxical increase in RBC-NOS activity [48]. In addition, shear stress, by increasing Ca 2?…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide synthetic pathway and cGMP levels are altered in red blood cells from end-stage renal disease patients

et al. 2016

View full text Add to dashboard Cite

Red blood cells (RBCs) enzymatically produce nitric oxide (NO) by a functional RBC-nitric oxide synthase (RBC-NOS). NO is a vascular key regulatory molecule. In RBCs its generation is complex and influenced by several factors, including insulin, acetylcholine, and calcium. NO availability is reduced in end-stage renal disease (ESRD) and associated with endothelial dysfunction. We previously demonstrated that, through increased phosphatidylserine membrane exposure, ESRD-RBCs augmented their adhesion to human cultured endothelium, in which NO bioavailability decreased. Since RBC-NOS-dependent NO production in ESRD is unknown, this study aimed to investigate RBC-NOS levels/activation, NO production/bioavailability in RBCs from healthy control subjects (C, N = 18) and ESRD patients (N = 27). Although RBC-NOS expression was lower in ESRDRBCs, NO, cyclic guanosine monophosphate (cGMP), RBC-NOS Serine1177 phosphorylation level and eNOS/ Calmodulin (CaM)/Heat Shock Protein-90 (HSP90) interaction levels were higher in ESRD-RBCs, indicating increased enzyme activation. Conversely, following RBCs stimulation with insulin or ionomycin, NO and cGMP levels were significantly lower in ESRD-than in C-RBCs, suggesting that uremia might reduce the RBC-NOS response to further stimuli. Additionally, the activity of multidrug-resistance-associated protein-4 (MRP4; cGMPmembrane transporter) was significantly lower in ESRDRBCs, suggesting a possible compromised efflux of cGMP across the ESRD-RBCs membrane. This study for the first time showed highest basal RBC-NOS activation in ESRDRBCs, possibly to reduce the negative impact of decreased NOS expression. It is further conceivable that high NO production only partially affects cell function of ESRDRBCs maybe because in vivo they are unable to respond to physiologic stimuli, such as calcium and/or insulin.Keywords End-stage renal disease Á Red blood cells Á Nitric oxide Á cGMP Á Nitric oxide synthase Mario Bonomini, and Assunta Pandolfi have contributed equally to the study.Electronic supplementary material The online version of this article

show abstract

Section: Discussionmentioning

confidence: 99%

Nitric oxide synthetic pathway and cGMP levels are altered in red blood cells from end-stage renal disease patients

et al. 2016

View full text Add to dashboard Cite

show abstract

“…The excess amount of these unpaired electrons destroys cellular lipids, proteins, and nucleic acids that have a role in different biological processes (Pruchniak et al 2016). However, the overproduction of reactive oxygen species accelerates the incidence or complications of disorders for example diabetes mellitus, cardiovascular diseases, diabetic nephropathy, Alzheimer's disease, and Parkinson's disease (Popolo et al 2013). Several studies have shown the correlation between oxidative stress and the pathogenesis of both major types of diabetes as well as the development of diabetic complications (Yang et al 2011, Giacco & Brownlee 2010.…”

Section: Introductionmentioning

confidence: 99%

Recurrent insulin-induced hypoglycemia induces AngII and COX2 leading to renal (pro)renin receptor expression and oxidative stress

Alanazi¹,

Uddin²,

Fakhruddin

et al. 2017

IJM

View full text Add to dashboard Cite

Background: Recurrent insulin-induced hypoglycemia (RIIH) is an avoidable consequence in the therapeutic management of diabetes mellitus. RIIH has been implicated in causing hypertension through an increase in renal and systemic AngII production. Objective: The present study was performed to assess the hypothesis that chronic insulin treatment enhances AngII and COX2 formation which in turn increases (pro) renin receptor (PRR) expression and NADPH oxidase-mediated oxidative stress, leading to renal and cardiac injury. Methods:The present studies were conducted in Male Sprague Dawley rats treated with daily subcutaneous injections of 7u/kg insulin or saline for 14 days. On the 14th day, surgery was performed for treatment infusion (captopril 12mg/kg, NS398 0.3mg/kg or vehicle), and renal interstitial fluid sample and urine collections for biomarker measurements. At the end of the experiments, kidneys and hearts were harvested to evaluate PRR and NOX2 (NADPH oxidase subunit) expression and oxidative stress. Results: We found that RIIH enhanced AngII and COX2 activity, leading to renal PRR expression and NADPH oxidase-induced oxidative stress in the heart and kidney. 8-isoprostane was evaluated as a renal biomarker of oxidative stress, which was induced in insulin treated animals and modulated by captopril and NS398. In addition, there was a slight increase in NGAL, a urinary biomarker of acute kidney injury (AKI), in insulin treated animals when compared to control. Conclusion: These results demonstrate that RIIH induces renal PRR expression and oxidative stress through increasing AngII and COX2 in the heart and kidney, leading to end-organ damage.

show abstract

“…The animals were placed in a heated chamber at an ambient temperature of 30-34 °C for 15 min and blood pressure values (1)(2)(3)(4)(5)(6)(7)(8)(9) were recorded for each animal. The lowest three readings were averaged to calculate the mean blood pressure.…”

Section: Blood Pressure Measurementsmentioning

confidence: 99%

“…Increased levels of reactive oxygen species such as superoxide anion, hydrogen peroxide and lipid peroxides are reported in patients with hypertension [3,4]. Arterial hypertension is often associated with pathologies related with oxidative stress and may be considered as a result of systemic damage in different target organs or tissues induced by free radicals [5,6]. Angiotensin Converting Enzyme (ACE) inhibitors have taken their place in clinical use as effective and safe antihypertensives and vascular protective agents [7].…”

Section: Introductionmentioning

confidence: 99%

Effects of lisinopril on oxidative stress in brain tissues of rats with L-NAME induced hypertension

Kırbaş¹,

Kutluhan²,

Kırbaş³

et al. 2013

Turk J Bioch

View full text Add to dashboard Cite

Objective: Arterial hypertension is often associated with pathologies related with oxidative stress. Angiotensin converting enzyme (ACE) inhibitors have been used as a safe and effective treatment of hypertension and coronary heart disease. However, the significance of ACE inhibitor usage in hypertension-induced cerebrovascular and neurodegenerative diseases is still unknown. In this study, we aimed to investigate the effects of lisinopril, an ACE inhibitor, on oxidative stress and antioxidant enzyme activities in brain tissues of rats with L-NAME (N ω -Nitro-L-Arginine Methyl Ester hydrochloride) induced hypertension. Methods: Thirty-two Sprague-Dawley rats were divided into four groups: Control, L-NAME, L-NAME plus lisinopril, and only lisinopril. Hypertension was induced by oral administration of the L-NAME (75 mg/kg/day) in drinking water for 6 weeks. Rats were treated with Lisinopril (10 mg/kg/day) for six weeks. Systolic blood pressures were measured at the first, third and sixth weeks by using tail cuff method. Malondialdehyde (MDA), Superoxide dismutase (SOD), Catalase (CAT) and Glutathione peroxidase (GSH-Px) activity were measured from the brain tissue. Nitric oxide (NO) levels were measured from plasma. Results: Our results showed that L-NAME leads to an increase in systolic blood pressure of animals. The antihypertensive effect of lisinopril was observed. MDA level was significantly increased, and antioxidant enzymes activities were decreased in L-NAME given group (p<0.05). However, there was no statistically significant differences between the lisinopril given and other groups according to antioxidant enzymes activities (p>0.05). Conclusion: In our study, hypertension led to oxidative damage in brain tissues. Although lisinopril prevents the hypertension induced oxidative damage, direct antioxidant effect was not observed. Further studies are needed in order to gain certainty effect of lisinopril in brain tissue.

show abstract

Oxidative stress in patients with cardiovascular disease and chronic renal failure

Cited by 145 publications

References 100 publications

Nitric oxide synthetic pathway and cGMP levels are altered in red blood cells from end-stage renal disease patients

Nitric oxide synthetic pathway and cGMP levels are altered in red blood cells from end-stage renal disease patients

Recurrent insulin-induced hypoglycemia induces AngII and COX2 leading to renal (pro)renin receptor expression and oxidative stress

Effects of lisinopril on oxidative stress in brain tissues of rats with L-NAME induced hypertension

Contact Info

Product

Resources

About