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      Comparison of the Ameliorating Effects of Valsartan and Amlodipine on Vascular Endothelial Dysfunction and Oxidative Stress in Elderly Patients with Type H Hypertension

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      Evidence-based Complementary and Alternative Medicine : eCAM
      Hindawi

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          Abstract

          Objective

          To explore whether long-term administration of valsartan or amlodipine can improve vascular endothelial function and reduce the production of reactive oxygen species in patients with H-type hypertension, so as to provide a reference for clinical treatment.

          Methods

          A total of 82 elderly patients with type H hypertension who were admitted to our hospital from March to August 2017 were selected as the research subjects. The study included a 4-week continuous irrigation period followed by a 24-week randomized treatment period. Forty patients in the valsartan group and 42 in the amlodipine group were treated with 5 mg amlodipine or 80 mg valsartan for 24 weeks. Clinical efficacy, 24 h mean DBP, SBP, and 24HSBP, DBP coefficient of variation, cardiac fatty acid-binding protein (H-FABP), vascular pseudohemophilia factor (VWF), nitric oxide (NO), endothelium-dependent vasodilation function (FMD), nonendothelium-dependent vasodilation function (NMD), malondialdehyde (MDA), GSH-Px, and SOD levels were observed.

          Results

          The total effective rate was 80.0% (32/40) in the valsartan group and 85.71% (36/42) in the amlodipine group, and the difference was not statistically significant ( P > 0.05). After 24 weeks of treatment, the 24 h mean SBP, SDP, 24HSBP, and DBP variation coefficients of the two groups were significantly decreased, and there was no statistical significance between the two groups ( P > 0.05). After treatment, the values of H-FABP, VWF, NO, and MDA in both groups decreased compared with before treatment, while the values of FMD%, NMD%, SOD, and GSH-Px increased compared with before treatment ( P > 0.05), and the levels of H-FABP, VWF, and NO in the valsartan group were lower than those in the amlodipine group. Meanwhile, FMD%, NMD%, SOD, and GSH-Px levels were higher than those in the amlodipine group ( P > 0.05).

          Conclusion

          Valsartan and amlodipine reduce blood pressure, improve vascular endothelial function, and inhibit oxidative stress in elderly patients with H-type hypertension on average. However, valsartan has a better effect on vascular endothelial dysfunction and oxidative stress in elderly patients with H-type hypertension.

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          Most cited references17

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          Oxidative Stress and Hypertension.

          A link between oxidative stress and hypertension has been firmly established in multiple animal models of hypertension but remains elusive in humans. While initial studies focused on inactivation of nitric oxide by superoxide, our understanding of relevant reactive oxygen species (superoxide, hydrogen peroxide, and peroxynitrite) and how they modify complex signaling pathways to promote hypertension has expanded significantly. In this review, we summarize recent advances in delineating the primary and secondary sources of reactive oxygen species (nicotinamide adenine dinucleotide phosphate oxidases, uncoupled endothelial nitric oxide synthase, endoplasmic reticulum, and mitochondria), the posttranslational oxidative modifications they induce on protein targets important for redox signaling, their interplay with endogenous antioxidant systems, and the role of inflammasome activation and endoplasmic reticular stress in the development of hypertension. We highlight how oxidative stress in different organ systems contributes to hypertension, describe new animal models that have clarified the importance of specific proteins, and discuss clinical studies that shed light on how these processes and pathways are altered in human hypertension. Finally, we focus on the promise of redox proteomics and systems biology to help us fully understand the relationship between ROS and hypertension and their potential for designing and evaluating novel antihypertensive therapies.
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            Vascular Endothelial Growth Factor Receptor 3 Regulates Endothelial Function Through β-Arrestin 1

            Receptor signaling is central to vascular endothelial function and is dysregulated in vascular diseases such as atherosclerosis and pulmonary arterial hypertension (PAH). Signaling pathways involved in endothelial function include vascular endothelial growth factor receptors (VEGFRs) and G protein-coupled receptors (GPCRs), which classically activate distinct intracellular signaling pathways and responses. The mechanisms that regulate these signaling pathways have not been fully elucidated and it is unclear what nodes for crosstalk exist between these diverse signaling pathways. For example, multifunctional β-arrestin (ARRB) adapter proteins are best known as regulators of GPCR signaling but their role at other receptors and their physiological importance in the setting of vascular disease is unclear. We used a combination of human samples from PAH, human microvascular endothelial cells from lung, and Arrb knockout mice to determine the role of ARRB1 in endothelial VEGFR3 signaling. Additionally, a number of biochemical analyses were performed to determine the interaction between ARRB1 and VEGFR3, signaling mediators downstream of VEGFR3, and the internalization of VEGFR3. Expression of ARRB1 and VEGFR3 was reduced in human PAH and deletion of Arrb1 in mice exposed to hypoxia led to worse PAH with a loss of VEGFR3 signaling. Knockdown of ARRB1 inhibited VEGF-C-induced endothelial cell proliferation, migration and tube formation, along with reduced VEGFR3, Akt and eNOS phosphorylation. This regulation was mediated by direct ARRB1 binding to the VEGFR3 kinase domain and resulted in decreased VEGFR3 internalization. Our results demonstrate a novel role for ARRB1 in VEGF receptor regulation and suggests a mechanism for cross-talk between GPCRs and VEGFRs in PAH. These findings also suggest that strategies to promote ARRB1-mediated VEGFR3 signaling could be useful in the treatment of pulmonary hypertension and other vascular disease.
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              Omega-3 polyunsaturated fatty acids improve endothelial function in humans at risk for atherosclerosis: A review.

              Epidemiology studies and clinical trials show that omega-3 polyunsaturated fatty acids (n-3 PUFAs) can prevent atherosclerotic morbidity and evidence suggests this may be mediated by improving endothelial dysfunction. Endothelial dysfunction is characterized by reduced vasodilation and a pro-inflammatory, pro-thrombotic state, and is an early pathological event in the development of atherosclerosis. Flow-mediated dilation (FMD), a gold standard for assessing endothelial dysfunction, is a predictor of future cardiovascular events and coronary heart disease risk. Notably, risk factors for endothelial dysfunction include classic risk factors for atherosclerosis: Elevated lipids, diabetes, hypertension, elevated BMI, cigarette smoking, and metabolic syndrome. In this paper, we review the ability of n-3 PUFAs to improve endothelial dysfunction in individuals with classic risk factors for atherosclerosis, but lacking diagnosed atherosclerotic disease, with the goal of identifying those individuals that might gain the most vasoprotection from n-3 PUFA supplements. We include trials using eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), or alpha-linolenic acid (ALA) alone, or EPA+DHA; and assessing endothelial function by FMD, forearm blood flow, or peripheral arterial tonometry. We found that n-3 PUFAs improved endothelial dysfunction in 16 of 17 studies in individuals with hyperlipidemia, elevated BMI, metabolic syndrome, or that smoked cigarettes, but only in 2 of 5 studies in diabetics. Further, these trials showed that use of EPA+DHA consistently improve endothelial dysfunction; ALA-enriched diets appear promising; but use of EPA or DHA alone requires further study. We conclude that individuals with hyperlipidemia, elevated BMI, metabolic syndrome, or that smoke could derive vaosprotective benefits from EPA+DHA supplementation.
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                Author and article information

                Contributors
                Journal
                Evid Based Complement Alternat Med
                Evid Based Complement Alternat Med
                ECAM
                Evidence-based Complementary and Alternative Medicine : eCAM
                Hindawi
                1741-427X
                1741-4288
                2022
                8 August 2022
                8 August 2022
                : 2022
                : 5054511
                Affiliations
                Department of Geriatrics, The First People's Hospital of Lianyungang, Lianyungang, Jiangsu, 222000, China
                Author notes

                Academic Editor: Fenglin Liu

                Author information
                https://orcid.org/0000-0003-2786-7459
                Article
                10.1155/2022/5054511
                9377898
                31e0a414-fd64-48ab-8300-02bd64b4d6b3
                Copyright © 2022 Lijuan Zhang et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 22 April 2022
                : 27 June 2022
                Categories
                Research Article

                Complementary & Alternative medicine
                Complementary & Alternative medicine

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