Molecular Mechanisms of Sodium-Sensitive Hypertension in the Metabolic Syndrome

Nizar, Jonathan M.; Bhalla, Vivek

doi:10.1007/s11906-017-0759-5

Cited by 14 publications

(12 citation statements)

References 126 publications

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“…Despite the large body of clinical evidences, molecular mechanisms leading to the development of MetS remain to be fully elucidated, even though chronic low-grade inflammation seems to play a critical role. 2 Even the role of adipose tissue is currently challenging, as different depots are associated with different and heterogeneous phenotypes, each one associated with different degree of CV risk. 3 In the light of this, there is matter for more specific investigations targeting different CV risk factors and their pathophysiological roles, especially when they are combined with each other.…”

Section: Introductionmentioning

confidence: 99%

Baseline hs‐CRP predicts hypertension remission in metabolic syndrome

Carbone

Elia

Casula

et al. 2019

Eur J Clin Investigation

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Background: Inflammation, overweight and other cardiovascular risk factors might negatively impact on hypertension remission in metabolic syndrome (MetS), independently of the pharmacological treatment. Here, the potential influence of systemic inflammation (assessed by serum high-sensitivity C-reactive protein [hs-CRP]) on hypertension remission will be investigated in a cohort of hypertensive patients with MetS. Material and Methods: Hypertensive patients with MetS (n = 100) were enrolled, treated under current behavior/dietary/pharmacological recommendations and followed up for 12 months. All patients received medications and nutritional advice based on Mediterranean-like dietary pattern in addition to psychological and physicalactivity counselling. At baseline (T0), 6 (T1) and 12 (T2) months of follow-up, clinical data, haematological and biochemical profiles and serum hs-CRP were measured. Results: As compared to T0, at T2 patients displayed improvements in anthropometric and metabolic profiles. At T2, the hypertension remission rate was 13.0%. Serum hs-CRP did not change overtime in the overall cohort. Surprisingly, patients who experienced hypertension remission were less treated with antihypertensive drugs, but developed a weak improvement in anthropometric measures during follow-up.The hypertension remission group had lower baseline levels of hs-CRP as compared to non-remission. Low baseline hs-CRP (<2 µg/mL, cut-off value identified by ROC curve) predicted hypertension remission, independently of antihypertensive treatment implementation, baseline systolic blood pressure and waist circumference improvement. Conclusions: Remission of hypertension in MetS is independently associated with baseline low CRP levels, which might suggest a critical role for inflammation in sustaining high blood pressure levels. K E Y W O R D SC-reactive protein, hypertension, inflammation, metabolic syndrome, obesity, overweight

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Section: Introductionmentioning

confidence: 99%

Baseline hs‐CRP predicts hypertension remission in metabolic syndrome

Carbone

Elia

Casula

et al. 2019

Eur J Clin Investigation

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“…The best known mechanisms of salt-sensitive hypertension in obesity and metabolic syndrome are altered hemodynamics, impaired Na + homeostasis, renal dysfunction, autonomic nervous system imbalance, endocrine alterations, oxidative stress and inflammation, and vascular injury [4]. These factors integrate interdependently to regulate salt transport in the kidney, leading to hypertension and enhanced salt sensitivity.…”

Section: Introductionmentioning

confidence: 99%

“…These factors integrate interdependently to regulate salt transport in the kidney, leading to hypertension and enhanced salt sensitivity. Based on Dr. Arthur Guyton’s quantitative mathematical model, the final common pathway for engendering hypertension is decreased renal salt excretion, which expands the blood volume and increases systemic blood pressure (BP) to excrete excess salt to achieve steady-state [4,5,6,7,8]. The mechanisms of salt-sensitive hypertension continue to be contentious and the subject of considerable interest, especially in obesity and metabolic syndrome due to the risk factor clustering [8,9].…”

Section: Introductionmentioning

confidence: 99%

Metabolic Syndrome and Salt-Sensitive Hypertension in Polygenic Obese TALLYHO/JngJ Mice: Role of Na/K-ATPase Signaling

Yan

Wang

Chaudhry

et al. 2019

IJMS

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We have demonstrated that Na/K-ATPase acts as a receptor for reactive oxygen species (ROS), regulating renal Na+ handling and blood pressure. TALLYHO/JngJ (TH) mice are believed to mimic the state of obesity in humans with a polygenic background of type 2 diabetes. This present work is to investigate the role of Na/K-ATPase signaling in TH mice, focusing on susceptibility to hypertension due to chronic excess salt ingestion. Age-matched male TH and the control C57BL/6J (B6) mice were fed either normal diet or high salt diet (HS: 2, 4, and 8% NaCl) to construct the renal function curve. Na/K-ATPase signaling including c-Src and ERK1/2 phosphorylation, as well as protein carbonylation (a commonly used marker for enhanced ROS production), were assessed in the kidney cortex tissues by Western blot. Urinary and plasma Na+ levels were measured by flame photometry. When compared to B6 mice, TH mice developed salt-sensitive hypertension and responded to a high salt diet with a significant rise in systolic blood pressure indicative of a blunted pressure-natriuresis relationship. These findings were evidenced by a decrease in total and fractional Na+ excretion and a right-shifted renal function curve with a reduced slope. This salt-sensitive hypertension correlated with changes in the Na/K-ATPase signaling. Specifically, Na/K-ATPase signaling was not able to be stimulated by HS due to the activated baseline protein carbonylation, phosphorylation of c-Src and ERK1/2. These findings support the emerging view that Na/K-ATPase signaling contributes to metabolic disease and suggest that malfunction of the Na/K-ATPase signaling may promote the development of salt-sensitive hypertension in obesity. The increased basal level of renal Na/K-ATPase-dependent redox signaling may be responsible for the development of salt-sensitive hypertension in polygenic obese TH mice.

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“…The risk factors associated with the presence of hypertension are age [4], weight [5], genotype [6], gender and race [7]. SAH pathophysiology is also complex, and some hypotheses explain the clinical findings in patients with hypertension; for example, increase in the activity of the sympathetic nervous system [8,9], salt sensitivity [10,11], increased arterial tone and vascular remodeling, arterial stiffness [12], and renin-angiotensin-aldosterone system overactivation [13,14].…”

Section: Introductionmentioning

confidence: 99%

Spirulina maxima Decreases Endothelial Damage and Oxidative Stress Indicators in Patients with Systemic Arterial Hypertension: Results from Exploratory Controlled Clinical Trial

Martínez-Sámano

Luqueño-Bocardo

et al. 2018

Marine Drugs

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(1) Background: Spirulina (Arthrospira) maxima has shown beneficial effects such as being anti-dyslipidemic, antiviral, antioxidant and antihypertensive. However, there are few and limited clinical studies. (2) Methods: a prospective, randomized, parallel pilot study of 4.5 g administration of Spirulina maxima or placebo for 12 weeks in 16 patients with systemic arterial hypertension (SAH) undergoing treatment with angiotensin-converting enzyme (ACE) inhibitors was performed to assess the effects on endothelial damage and oxidative stress indicators. The blood levels of sICAM-1, sVCAM-1, endothelin-1, and sE-selectin were quantified; the activities of catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase and concentrations of reduced glutathione, oxidized glutathione, and thiobarbituric acid reactive substances, were also quantified before and after the treatment period. (3) Results: There were statistically significant (p < 0.05) decreases in systolic blood pressure, sVCAM-1, sE-selectin and endothelin-1 levels, and increases in glutathione peroxidase activity and oxidized glutathione levels. (4) Conclusion: The effects found in the present study agree with antihypertensive and antioxidant effects previously reported for Spirulina maxima. However, this is the first report about the effects on indicators of endothelial damage. More research in this field is necessary to gain an insight into the effects of Spirulina on these indicators.

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Molecular Mechanisms of Sodium-Sensitive Hypertension in the Metabolic Syndrome

Cited by 14 publications

References 126 publications

Baseline hs‐CRP predicts hypertension remission in metabolic syndrome

Baseline hs‐CRP predicts hypertension remission in metabolic syndrome

Metabolic Syndrome and Salt-Sensitive Hypertension in Polygenic Obese TALLYHO/JngJ Mice: Role of Na/K-ATPase Signaling

Spirulina maxima Decreases Endothelial Damage and Oxidative Stress Indicators in Patients with Systemic Arterial Hypertension: Results from Exploratory Controlled Clinical Trial

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