Exogenous l-arginine reduces matrix metalloproteinase-2 and -9 activities and oxidative stress in patients with hypertension

Garcia, Vinicius P; Rocha, Helena; Silva, Gustavo M.; T, Amaral; Secher, Niels H.; Nóbrega, Antônio Cláudio Lucas da; Vianna, Lauro C.; Rocha, Nazareth de Novaes

doi:10.1016/j.lfs.2016.06.006

Cited by 16 publications

(5 citation statements)

References 63 publications

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“…The two markers analyzed for lipid oxidation in this study, 15-F 2t -isoprostane and MDA, were measured in urine. 15-F 2t -isoprostane was significantly elevated in the hypertensive groups, as was reported before in some studies (e.g., [26,27]). Adjustment for age led to a loss of a difference between the hypertensive groups and the controls, as also observed before [28,29].…”

Section: Discussionsupporting

confidence: 86%

Differential Modulation of Markers of Oxidative Stress and DNA Damage in Arterial Hypertension

Kreutzmann,

Kraus,

Christa

et al. 2023

Antioxidants

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Patients with arterial hypertension have an increased risk of developing tumors, particularly renal cell carcinoma. Arterial hypertension is linked to DNA damage via the generation of oxidative stress, in which an upregulated renin–angiotensin–aldosterone system plays a crucial role. The current study investigated surrogates of oxidative stress and DNA damage in a group of hypertensive patients (HypAll, n = 64) and subgroups of well (HypWell, n = 36) and poorly (HypPoor, n = 28) controlled hypertensive patients compared to healthy controls (n = 8). In addition, a longitudinal analysis was performed with some of the hypertensive patients. Markers for oxidative stress in plasma (SHp, D-ROM, and 3-nitrotyrosine) and urine (8-oxodG, 15-F2t-isoprostane, and malondialdehyde) and markers for DNA damage in lymphocytes (γ-H2AX and micronuclei) were measured. In HypAll, all markers of oxidative stress except malondialdehyde were increased compared to the controls. After adjustment for age, this association was maintained for the protein stress markers SHp and 3-nitrotyrosine. With regard to the markers for DNA damage, there was no difference between HypAll and the controls. Further, no significant differences became apparent in the levels of both oxidative stress and DNA damage between HypWell and HypPoor. Finally, a positive correlation between the development of blood pressure and oxidative stress was observed in the longitudinal study based on the changes in D-ROM and systolic blood pressure. In conclusion, we found increased oxidative stress in extensively treated hypertensive patients correlating with the level of blood-pressure control but no association with DNA damage.

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Section: Discussionsupporting

confidence: 86%

Differential Modulation of Markers of Oxidative Stress and DNA Damage in Arterial Hypertension

Kreutzmann,

Kraus,

Christa

et al. 2023

Antioxidants

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“…In contrast, arginine supplementation improved the impaired endothelium-dependent vasodilation in hypercholesterolaemic animals with endothelial dysfunction (84) . Previous studies have demonstrated that reactive O 2 species are associated with an impaired arginine-NO pathway in individuals with metabolic alterations (85)(86)(87)(88) . Considering the increased systemic and tissue-specific oxidative status observed in this experimental model (7) , this oxidative stress can adversely affect the action of NO and, consequently, vascular function.…”

Section: Vascular Functionmentioning

confidence: 99%

Arginine and aerobic training prevent endothelial and metabolic alterations in rats at high risk for the development of the metabolic syndrome

et al. 2017

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Endothelial function is a key mechanism in the development of CVD. Arginine and exercise are important non-pharmacological strategies for mitigating the impact of metabolic changes in the metabolic syndrome, but the effect of their combined administration is unknown. Thus, the aim of this study was to investigate the isolated and combined effects of aerobic training and arginine supplementation on metabolic variables and vascular reactivity in rats at high risk for developing the metabolic syndrome. Wistar rats were divided into two groups: control and fructose (F - water with 10 % fructose). After 2 weeks, the F group was divided into four groups: F, fructose+arginine (FA, 880 mg/kg per d of l-arginine), fructose+training (FT) and fructose+arginine+training (FTA); treatments lasted for 8 weeks, and no difference was observed in body mass gain. Arginine did not improve the body protein content, and both the FA and FT groups show a reversal of the increase in adipose tissue. Insulin increase was prevented by training and arginine, without additive effect, and the increase in serum TAG was prevented only by training. The F group showed impaired endothelium-dependent vasodilation and hyperreactivity to phenylephrine, but arginine and training were capable of preventing these effects, even separately. Higher nitric oxide level was observed in the FA and FT groups, and no potentiating effect was detected. Thus, only training was able to prevent the increase in TAG and improve the protein mass, and training and arginine exert similar effects on fat content, insulin and endothelial function, but these effects are not additive.

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“…Arterial and internal jugular venous blood plasma nitrite levels were determined via the chemiluminescence reaction of NO with ozone conducted by an NO analyser (Sievers, Boulder, CO, USA) (Garcia et al 2016). Briefly, blood was sampled into trace metal-free tubes containing sodium heparin.…”

Section: Plasma Nitritementioning

confidence: 99%

Human brain blood flow and metabolism during isocapnic hyperoxia: the role of reactive oxygen species

Mattos

Campos

Rocha

et al. 2018

The Journal of Physiology

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Key points It is unknown whether excessive reactive oxygen species (ROS) production drives the isocapnic hyperoxia (IH)‐induced decline in human cerebral blood flow (CBF) via reduced nitric oxide (NO) bioavailability and leads to disruption of the blood–brain barrier (BBB) or neural‐parenchymal damage. Cerebral metabolic rate for oxygen (CMRnormalO2) and transcerebral exchanges of NO end‐products, oxidants, antioxidants and neural‐parenchymal damage markers were simultaneously quantified under IH with intravenous saline and ascorbic acid infusion. CBF and CMR normalO2 were reduced during IH, responses that were followed by increased oxidative stress and reduced NO bioavailability when saline was infused. No indication of neural‐parenchymal damage or disruption of the BBB was observed during IH. Antioxidant defences were increased during ascorbic acid infusion, while CBF, CMR normalO2, oxidant and NO bioavailability markers remained unchanged. ROS play a role in the regulation of CBF and metabolism during IH without evidence of BBB disruption or neural‐parenchymal damage. Abstract To test the hypothesis that isocapnic hyperoxia (IH) affects cerebral blood flow (CBF) and metabolism through exaggerated reactive oxygen species (ROS) production, reduced nitric oxide (NO) bioavailability, disturbances in the blood–brain barrier (BBB) and neural‐parenchymal homeostasis, 10 men (24 ± 1 years) were exposed to a 10 min IH trial (100% O2) while receiving intravenous saline and ascorbic acid (AA, 3 g) infusion. Internal carotid artery blood flow (ICABF), vertebral artery blood flow (VABF) and total CBF (tCBF, Doppler ultrasound) were determined. Arterial and right internal jugular venous blood was sampled to quantify the cerebral metabolic rate of oxygen (CMRnormalO2), transcerebral exchanges (TCE) of NO end‐products (plasma nitrite), antioxidants (AA and AA plus dehydroascorbic acid (AA+DA)) and oxidant biomarkers (thiobarbituric acid‐reactive substances (TBARS) and 8‐isoprostane), and an index of BBB disruption and neuronal‐parenchymal damage (neuron‐specific enolase; NSE). IH reduced ICABF, tCBF and CMR normalO2, while VABF remained unchanged. Arterial 8‐isoprostane and nitrite TCE increased, indicating that CBF decline was related to ROS production and reduced NO bioavailability. AA, AA+DA and NSE TCE did not change during IH. AA infusion did not change the resting haemodynamic and metabolic parameters but raised antioxidant defences, as indicated by increased AA/AA+DA concentrations. Negative AA+DA TCE, unchanged nitrite, reductions in arterial and venous 8‐isoprostane, and TBARS TCE indicated that AA infusion effectively inhibited ROS production and preserved NO bioavailability. Similarly, AA infusion prevented IH‐induced decline in regional and total CBF and re‐established CMR normalO2. These findings indicate that ROS play a role in CBF regulation and metabolism during IH without evidence of BBB disruption or neural‐parenchymal damage.

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Exogenous l-arginine reduces matrix metalloproteinase-2 and -9 activities and oxidative stress in patients with hypertension

Cited by 16 publications

References 63 publications

Differential Modulation of Markers of Oxidative Stress and DNA Damage in Arterial Hypertension

Differential Modulation of Markers of Oxidative Stress and DNA Damage in Arterial Hypertension

Arginine and aerobic training prevent endothelial and metabolic alterations in rats at high risk for the development of the metabolic syndrome

Human brain blood flow and metabolism during isocapnic hyperoxia: the role of reactive oxygen species

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