scholarly journals Új szempontok a sószenzitív hypertoniák patomechanizmusában

2019 ◽  
Vol 160 (2) ◽  
pp. 43-49
Author(s):  
Endre Sulyok
Keyword(s):  
Blood Pressure ◽  
Extracellular Space ◽  
Salt Intake ◽  
Sodium Intake ◽  
Organ Damage ◽  
Blood Pressure Elevation ◽  
High Sodium ◽  
End Organ Damage ◽  
Inactive Form ◽  
Factor C

Abstract: This article shortly outlines the evolution of hypertonia from risk factors to end-organ damage. The pathogenetic role of salt intake is underlined and in the light of recent clinical and experimental observations, the importance of renal and extrarenal mechanism in the development of salt-sensitive hypertension is analysed. The generally accepted concept that the inefficient renal sodium excretion and the subsequent expansion of the extracellular space is the major factor in blood pressure elevation is challenged. Evidences have been provided that the retained sodium dissociates from the volume of extracellular space and, also from the blood pressure. It has been shown that the negatively charged macromolecules in the subcutaneous interstitium bind sodium ions in osmotically inactive form and store sodium reversibly. The local tissue hypertonicity induces monocytes/macrophages invasion and activation that causes increased expression of tonicity-responsive enhancer binding protein (TonEBP) and the secretion of vascular endothelial growth factor C that result in enhanced lymphangiogenesis. The expanded lymphatic system drains the excess sodium and volume back to the circulation. The reduction of buffer function of this system may contribute to the development or to worsening of hypertension. Similar buffer and barrier functions are attributed to the glycocalyx that covers the luminal surface of vascular endothelium. It is also recognised that the high sodium intake alone is an important pathogenetic factor in end-organ damage independent of hypertension. This may be accounted for by the induction and activation of Th17 cells as well as by the increased production of several pro-inflammatory and pro-fibrotic cytokines. Orv Hetil. 2019; 160(2): 43–49.

scholarly journals Sodium Intake and Hypertension

Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 1970 ◽  
Author(s):  
Grillo ◽  
Salvi ◽  
Coruzzi ◽  
Salvi ◽  
Parati
Keyword(s):  
Blood Pressure ◽  
Salt Intake ◽  
Sodium Intake ◽  
Peripheral Resistance ◽  
Dietary Sodium ◽  
Dietary Salt ◽  
High Sodium ◽  
Close Relationship ◽  
And Function ◽  
Modest Reduction

The close relationship between hypertension and dietary sodium intake is widely recognized and supported by several studies. A reduction in dietary sodium not only decreases the blood pressure and the incidence of hypertension, but is also associated with a reduction in morbidity and mortality from cardiovascular diseases. Prolonged modest reduction in salt intake induces a relevant fall in blood pressure in both hypertensive and normotensive individuals, irrespective of sex and ethnic group, with larger falls in systolic blood pressure for larger reductions in dietary salt. The high sodium intake and the increase in blood pressure levels are related to water retention, increase in systemic peripheral resistance, alterations in the endothelial function, changes in the structure and function of large elastic arteries, modification in sympathetic activity, and in the autonomic neuronal modulation of the cardiovascular system. In this review, we have focused on the effects of sodium intake on vascular hemodynamics and their implication in the pathogenesis of hypertension.

Salt, Frusemide and Renin in Severe Experimental Renal Hypertension

1976 ◽  
Vol 51 (s3) ◽  
pp. 129s-132s
Author(s):  
M. Fernandes ◽  
G. Onesti ◽  
R. Dykyj ◽  
R. Fiorentini ◽  
Anne B. Gould ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Early Phase ◽  
Sodium Intake ◽  
Renal Hypertension ◽  
Deficient Diet ◽  
Blood Pressure Elevation ◽  
High Sodium ◽  
High Sodium Intake ◽  
Experimental Renal Hypertension ◽  
High Sodium Diet

1. Sodium-deficient diet failed to alter development and maintenance of severe renal hypertension produced in the rat by ligation of the aorta between the renal arteries. 2. High sodium diet did not alter the early phase of this hypertension, but significantly decreased blood pressure elevation in the late phases. 3. The decrease in blood pressure produced by high sodium intake does not appear to be mediated by renin suppression. 4. Frusemide effectively reduced blood pressure and renin at all phases.

scholarly journals SKIN LYMPHATIC SYSTEM IN THE PATHOGENESIS OF ARTERIAL HYPERTENSION – REVIEW AND CRITIQUE

Lymphology ◽  
2021 ◽  
Vol 53 (3) ◽  
Author(s):  
A Chachaj ◽  
A Szuba
Keyword(s):  
Blood Pressure ◽  
Molecular Mechanisms ◽  
Lymphatic System ◽  
Salt Intake ◽  
Lymphatic Vessels ◽  
High Salt ◽  
Large Reservoir ◽  
Inactive Form ◽  
High Salt Intake ◽  
Factor C

Although numerous studies have confirmed the relationship between high salt intake and elevated blood pressure, the exact molecular mechanisms of this relationship are still unclear. There is growing evidence that skin interstitium, as well as the skin lymphatic system, are important regulators of both sodium (Na+) balance and blood pressure. Skin is in itself a large reservoir of Na+ ions which are stored in an osmotically inactive form on glycosaminoglycans (GAGs). Local hypertonicity due to extensive accumulation of Na+ within the skin as a result of a high-salt diet was demonstrated to induce macrophages to express a transcription factor termed tonicity-responsive enhancer binding protein (TonEBP) and subsequently to secrete vascular endothelial growth factor-C (VEGF-C), activating lymphangiogenesis within the skin. This regulatory axis seems to be adaptive in maintaining blood pressure in high salt-load states. Recent studies have added new insights into the functioning of lymphatic vessels and the pathogenesis of salt-sensitive hypertension as well as questioned the classic view of Na+ homeostasis. This review aims to summarize recent findings pertaining to the involvement of the skin lymphatic system in Na+ and blood pressure regulation.

Dietary Sodium Restriction in the Management of Chronic Kidney Disease: A Systematic Review and Meta-Analysis of RCTs

2021 ◽  
Author(s):  
Sai Sidharth Manikandan ◽  
Murali Dhar
Keyword(s):  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Salt Intake ◽  
Sodium Intake ◽  
Meta Analysis ◽  
Cost Effective ◽  
Mean Difference ◽  
Dietary Sodium ◽  
High Sodium

Abstract Background: Non-pharmacological strategies such as lowering sodium intake aim to protect renal function and delay the initiation of renal replacement therapy. It might also be a cost-effective method to improve chronic kidney disease (CKD) prognosis. We decided to perform a meta-analysis of randomized controlled trials (RCTs) to evaluate the effects of low versus high sodium intake in adults with CKD. Results:Our search strategy yielded seven studies from six countries with 465 participants. The overall effect on restricted sodium intake favored reduction in systolic blood pressure with an overall mean difference of -6.14(95% CI: -9.52, -2.76) and reduction in diastolic blood pressure with a mean difference of -3.08 (95% CI: -4.62, -1.55). There was lowering of estimated glomerular filtration rate (eGFR), however the same was not statistically significant.Conclusion:The study found that restricted salt intake could significantly reduce systolic and diastolic BP. Further, multi-center RCTs for longer durations across different stages of CKD could effectively assess the effects of restricted sodium intake on vital parameters. Such study designs could also help clinicians identify the optimal intake of dietary sodium to achieve better renal and cardio vascular outcomes.

scholarly journals The Impact of High Dietary Sodium Consumption on Blood Pressure Variability in Healthy, Young Adults

2020 ◽  
Vol 33 (5) ◽  
pp. 422-429 ◽  
Author(s):  
Kamila U Migdal ◽  
Matthew C Babcock ◽  
Austin T Robinson ◽  
Joseph C Watso ◽  
Megan M Wenner ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Variability ◽  
Salt Intake ◽  
Secondary Analysis ◽  
Organ Damage ◽  
Healthy Adults ◽  
Dietary Sodium ◽  
High Sodium ◽  
Ambulatory Bp Monitoring ◽  
The Impact

Abstract BACKGROUND High sodium (Na+) intake augments blood pressure variability (BPV) in normotensive rodents, without changes in resting blood pressure (BP). Augmented BPV is associated with end-organ damage and cardiovascular morbidity. It is unknown if changes in dietary Na+ influence BPV in humans. We tested the hypothesis that high Na+ feeding would augment BPV in healthy adults. METHODS Twenty-one participants (10 F/11 M; 26 ± 5 years; BP: 113 ± 11/62 ± 7 mm Hg) underwent a randomized, controlled feeding study that consisted of 10 days of low (2.6 g/day), medium (6.0 g/day), and high (18.0 g/day) salt diets. On the ninth day of each diet, 24-h urine samples were collected and BPV was calculated from 24-h ambulatory BP monitoring. On the tenth day, in-laboratory beat-to-beat BPV was calculated during 10 min of rest. Serum electrolytes were assessed. We calculated average real variability (ARV) and standard deviation (SD) as metrics of BPV. As a secondary analysis, we calculated central BPV from the 24-h ambulatory BP monitoring. RESULTS 24-h urinary Na+ excretion (low = 41 ± 24, medium = 97 ± 43, high = 265 ± 92 mmol/24 h, P < 0.01) and serum Na+ (low = 140.0 ± 2.1, medium = 140.7 ± 2.7, high = 141.7 ± 2.5 mmol/l, P = 0.009) increased with greater salt intake. 24-h ambulatory ARV (systolic BP ARV: low = 9.5 ± 1.7, medium = 9.5 ± 1.2, high = 10.0 ± 1.9 mm Hg, P = 0.37) and beat-to-beat ARV (systolic BP ARV: low = 2.1 ± 0.6, medium = 2.0 ± 0.4, high = 2.2 ± 0.8 mm Hg, P = 0.46) were not different. 24-h ambulatory SD (systolic BP: P = 0.29) and beat-to-beat SD (systolic BP: P = 0.47) were not different. There was a trend for a main effect of the diet (P = 0.08) for 24-h ambulatory central systolic BPV. CONCLUSIONS Ten days of high sodium feeding does not augment peripheral BPV in healthy, adults. CLINICAL TRIALS REGISTRATION NCT02881515.

scholarly journals Is too much salt harmful? Yes

2019 ◽  
Vol 35 (9) ◽  
pp. 1777-1785 ◽  
Author(s):  
Róbert Agócs ◽  
Dániel Sugár ◽  
Attila J. Szabó
Keyword(s):  
Blood Pressure ◽  
Salt Intake ◽  
Sodium Intake ◽  
Blood Pressure Reduction ◽  
Great Part ◽  
Risk Groups ◽  
Vulnerable Groups ◽  
High Sodium ◽  
Salt Consumption ◽  
Low Sodium Diet

AbstractThe contribution of high sodium intake to hypertension and to the severity of immune-mediated diseases is still being heatedly debated in medical literature and in the lay media. This review aims to demonstrate two conflicting views on the topic, with the first part citing the detrimental effects of excessive salt consumption. Sodium plays a central role in volume and blood pressure homeostasis, and the positive correlation between sodium intake and blood pressure has been extensively researched. Despite the fact that the average of global daily salt consumption exceeds recommendations of international associations, health damage from excessive salt intake is still controversial. Individual differences in salt sensitivity are in great part attributed to this contradiction. Patients suffering from certain diseases as well as other vulnerable groups—either minors or individuals of full age—exhibit more pronounced blood pressure reduction when consuming a low-sodium diet. Furthermore, findings from the last two decades give insight into the concept of extrarenal sodium storage; however, the long-term consequences of this phenomenon are lesser known. Evidence of the relationship between sodium and autoimmune diseases are cited in the review, too. Nevertheless, further clinical trials are needed to clarify their interplay. In conclusion, for salt-sensitive risk groups in the population, even stricter limits of sodium consumption should be set than for young, healthy individuals. Therefore, the question raised in the title should be rephrased as follows: “how much salt is harmful” and “for whom is elevated salt intake harmful?”

scholarly journals Immune mechanisms in arterial hypertension. Recent advances

2021 ◽  
Author(s):  
Ulrich O. Wenzel ◽  
Heimo Ehmke ◽  
Marlies Bode
Keyword(s):  
Blood Pressure ◽  
T Cells ◽  
Dendritic Cells ◽  
Immune System ◽  
Organ Damage ◽  
T Cell Subsets ◽  
Blood Pressure Elevation ◽  
End Organ Damage ◽  
Pressure Elevation ◽  
Recent Advances

AbstractIncreasing evidence indicates that hypertension and hypertensive end-organ damage are not only mediated by hemodynamic injury. Inflammation also plays an important role in the pathophysiology and contributes to the deleterious consequences of this disease. Cells of the innate immune system including monocyte/macrophages and dendritic cells can promote blood pressure elevation via effects mostly on kidney and vascular function. Moreover, convincing evidence shows that T and B cells from the adaptive immune system are involved in hypertension and hypertensive end-organ damage. Skin monocyte/macrophages, regulatory T cells, natural killer T cells, and myeloid-derived suppressor cells have been shown to exert blood pressure controlling effects. Sodium intake is undoubtedly indispensable for normal body function but can be detrimental when taken in excess of dietary requirements. Sodium levels also modulate the function of monocyte/macrophages, dendritic cells, and different T cell subsets. Some of these effects are mediated by changes in the microbiome and metabolome that can be found after high salt intake. Modulation of the immune response can reduce severity of blood pressure elevation and hypertensive end-organ damage in several animal models. The purpose of this review is to briefly summarize recent advances in immunity and hypertension as well as hypertensive end-organ damage.

Classic and Nonclassic Apparent Mineralocorticoid Excess Syndrome

2019 ◽  
Vol 105 (4) ◽  
pp. e924-e936 ◽  
Author(s):  
Cristian A Carvajal ◽  
Alejandra Tapia-Castillo ◽  
Andrea Vecchiola ◽  
Rene Baudrand ◽  
Carlos E Fardella
Keyword(s):  
Blood Pressure ◽  
Sodium Intake ◽  
Evidence Synthesis ◽  
Plasma Renin ◽  
Organ Damage ◽  
Second Hit ◽  
High Sodium ◽  
Endocrine Hypertension ◽  
Urinary Potassium ◽  
Apparent Mineralocorticoid Excess

Abstract Context Arterial hypertension (AHT) is one of the most frequent pathologies in the general population. Subtypes of essential hypertension characterized by low renin levels allowed the identification of 2 different clinical entities: aldosterone-mediated mineralocorticoid receptor (MR) activation and cortisol-mediated MR activation. Evidence Acquisition This review is based upon a search of Pubmed and Google Scholar databases, up to August 2019, for all publications relating to endocrine hypertension, apparent mineralocorticoid excess (AME) and cortisol (F) to cortisone (E) metabolism. Evidence Synthesis The spectrum of cortisol-mediated MR activation includes the classic AME syndrome to milder (nonclassic) forms of AME, the latter with a much higher prevalence (7.1%) than classic AME but different phenotype and genotype. Nonclassic AME (NC-AME) is mainly related to partial 11βHSD2 deficiency associated with genetic variations and epigenetic modifications (first hit) and potential additive actions of endogenous or exogenous inhibitors (ie, glycyrrhetinic acid-like factors [GALFS]) and other factors (ie, age, high sodium intake) (second hit). Subjects with NC-AME are characterized by a high F/E ratio, low E levels, normal to elevated blood pressure, low plasma renin and increased urinary potassium excretion. NC-AME condition should benefit from low-sodium and potassium diet recommendations and monotherapy with MR antagonists. Conclusion NC-AME has a higher prevalence and a milder phenotypical spectrum than AME. NC-AME etiology is associated to a first hit (gene and epigene level) and an additive second hit. NC-AME subjects are candidates to be treated with MR antagonists aimed to improve blood pressure, end-organ damage, and modulate the renin levels.

scholarly journals Dietary Sodium Restriction in the Management of Chronic Kidney Disease: A Meta-Analysis of RCTs

2021 ◽  
Vol 8 (2) ◽  
Author(s):  
Sai Sidharth M ◽  
◽  
Dhar M ◽  
Keyword(s):  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Salt Intake ◽  
Sodium Intake ◽  
Meta Analysis ◽  
Mean Difference ◽  
Dietary Sodium ◽  
Cochrane Library ◽  
High Sodium

Introduction: Non-pharmacological strategies such as lowering sodium intake aim to protect renal function and delay the initiation of renal replacement therapy. It might also be a cost-effective method to improve Chronic Kidney Disease (CKD) prognosis. We decided to perform a meta-analysis of Randomized Controlled Trials (RCTs) to evaluate the effects of low versus high sodium intake in adults with CKD. Methodology: We searched the online databases – PUBMED, Cochrane Kidney and Transplant Specialized Register, Cochrane Library and Google Scholar to 31st December 2020 for RCTs to be included in the study. Meta- Analysis was performed for the intervention groups for each arm against the control. Inverse variance methods were applied for analysis using random effects models due to the high heterogeneity among the studies. Results: Our search strategy yielded seven studies from six countries with 465 participants. The overall effect on restricted sodium intake favored reduction in systolic blood pressure with an overall mean difference of -6.14(95% CI: -9.52, -2.76) and reduction in diastolic blood pressure with a mean difference of -3.08 (95% CI: -4.62, -1.55). There was lowering of estimated Glomerular Filtration Rate (eGFR), however the same was not statistically significant. Conclusion: The study found that restricted salt intake could significantly reduce systolic and diastolic BP. Further, multi-center RCTs for longer durations across different stages of CKD could effectively assess the effects of restricted sodium intake on vital parameters. Such study designs could also help clinicians identify the optimal intake of dietary sodium to achieve better renal and cardio vascular outcomes.

Soybean proteins counteract heart remodeling in wistar rats fed a high sodium chloride diet

2019 ◽  
Vol 23 (6) ◽  
pp. 92-99
Author(s):  
I. G. Kayukov ◽  
O. N. Beresneva ◽  
M. M. Parastaeva ◽  
G. T. Ivanova ◽  
A. N. Kulikov ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Chloride ◽  
Cardiac Remodeling ◽  
Wistar Rats ◽  
Salt Intake ◽  
Left Ventricular ◽  
High Salt ◽  
Soy Proteins ◽  
High Sodium ◽  
Heart Remodeling

BACKGROUND. Increased salt intake is associated with a number of cardiovascular events, including increased blood pressure (BP) and the development of left ventricular hypertrophy (LVH). However, there is much evidence that a high content of sodium chloride in the diet does not always lead to an increase in BP, but almost inevitably causes cardiac remodeling, in particular, LVH. Many aspects of myocardial remodeling induced by high sodium content in the food have not been studied enough. THE AIM of the study was to trace the echocardiographic changes in Wistar rats fed the high salt ration and the high salt ration supplemented with soy proteins.MATERIAL AND METHODS. Echocardiography and BP measurements were performed on male Wistar rats, divided into three groups. The first (control; n = 8) included rats that received standard laboratory feed (20.16 % animal protein and 0.34 % NaCl); the second (n = 10) – animals that received standard feed and 8 % NaCl (high salt ration). The third group (n = 10) consisted of rats who consumed a low-protein diet containing 10 % soy protein isolate (SUPRO 760) and 8 % NaCl. The follow-up period was 2 and 4 months.THE RESULTS of the study showed that: (1) the intake of a large amount of salt with a diet does not necessarily lead to the formation of arterial hypertension; (2) despite the absence of a distinct increase in BP, under these conditions signs of cardiac remodeling, in particular, LVH, appear rather quickly; (3) supplementing a high-salt diet with soy isolates counteracts the development of LVH.CONCLUSION. High salt intake with food can cause heart remodeling, regardless of blood pressure, while soy proteins can counteract this process.

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