Hypertension Associated with Fructose and High Salt: Renal and Sympathetic Mechanisms

Komnenov, Dragana; Levanovich, Peter; Rossi, Noreen F.

doi:10.3390/nu11030569

Cited by 53 publications

(41 citation statements)

References 78 publications

(110 reference statements)

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“…Soncrant et al reported that elevated BP was increased by sympathoexcitation in 20% fructose-induced, salt-sensitive, hypertensive rats [33]. It has been shown that the ingestion of fructose altered the secretion of hormones that regulate energy balance associated with increased SNA [34]. However, in the current study, although a DGAT1 inhibitor was administered orally to block triglycerides production, sympathoexcitation was not inhibited in fructose-fed rats.…”

Section: Discussioncontrasting

confidence: 55%

Excessive Fructose Intake Impairs Baroreflex Sensitivity and Led to Elevated Blood Pressure in Rats

et al. 2019

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Hypertension development with an increased intake of added sugar, especially excessive fructose intake, was shown in the National Health and Nutrition Examination Survey (NHANES) data. However, the mechanism underlying blood pressure (BP) elevation with increased fructose intake is still unclear. First, the present study showed that in rats fed 10% fructose for one week, BP and fructose/glucose levels increased in the central and peripheral nervous system. Furthermore, increased fructose intake resulted in an upregulation of fructose concentration in the cerebrospinal fluid. Second, consumption of excess fructose increased serum triglycerides. However, the inhibition of triglyceride production did not mitigate sympathetic nerve hyperactivity, but contributed to an insignificant decrease in BP. Finally, increased fructose intake reduced nitric oxide (NO) levels in the nucleus tractus solitarii (NTS) and reduced baroreflex sensitivity within a week. Collectively, the data suggested that fructose intake reduced NO levels in the NTS and caused baroreflex dysfunction, which further stimulated sympathetic nerve activity and induced the development of high BP.

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Section: Discussioncontrasting

confidence: 55%

Excessive Fructose Intake Impairs Baroreflex Sensitivity and Led to Elevated Blood Pressure in Rats

et al. 2019

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“…Excess salt intake has been linked to many chronic diseases, including hypertension, cardiovascular disease, kidney dysfunction, and osteoporosis [2][3][4][5]. While an increase in salt-enriched "fast food" consumption has been considered a putative factor for many pathological conditions, there is no (animal or human) data available to delineate whether a long-term high-salt diet (HSD) may disturb pain sensitivity.…”

Section: Introductionmentioning

confidence: 99%

High-salt diet decreases mechanical thresholds in mice that is mediated by a CCR2-dependent mechanism

Fan

Oladiran

Shi

et al. 2020

J Neuroinflammation

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Background: Though it is well-known that a high-salt diet (HSD) is associated with many chronic diseases, the effects of long-term high-salt intake on physiological functions and homeostasis remain elusive. In this study, we investigated whether and how an HSD affects mouse nociceptive thresholds, and myeloid cell trafficking and activation. Methods: Healthy C57BL/6 male and female mice were fed an HSD (containing 4% NaCl in chow and 1% NaCl in water) from the time of weaning for 3 to 4 months. Circulating monocytes, nerve macrophages, spinal microglia, and associated inflammatory responses were scrutinized using flow cytometry, immunohistochemistry, and quantitative real-time polymerase chain reaction (qPCR) approaches. Mouse pain sensitivity to mechanical stimuli was monitored with von Frey tests along the experimental duration. Results: Mice on an HSD have reduced mechanical thresholds. They feel more pain than those on a normal diet (ND), e.g., regular laboratory chow (0.3% NaCl in chow). An HSD induced not only a remarkable expansion of circulating monocytes, CCR2 + Ly6C hi inflammatory monocytes in particular, but also an accumulation of CD11b + F4/ 80 + macrophages in the peripheral nerves and an activation of Iba-1 + spinal microglia. Replacing an HSD with a ND was unable to reverse the HSD-induced mechanical hypersensitivity or rescue the altered immune responses. However, treating HSD-fed mice with a chemokine receptor CCR2 antagonist effectively normalized the pain thresholds and immune cell profile in the periphery and spinal cord. An HSD failed to alter pain thresholds and myeloid cell activation in CCR2-deficient mice. Spinal microglial activation is required for HSD-induced mechanical hypersensitivity in male, but not in female mice. Conclusion: Overall, this study provides evidence that an HSD has a long-term impact on physiological function. CCR2-mediated cellular response, including myeloid cell trafficking and associated inflammation, plays pivotal roles in salt-dietary modulation of pain sensitivity.

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“…High-fructose corn syrup (HFCS) is the main source of added sweeteners in sweetened beverages. A high intake of HFCS causes an increase in BP and thus involves an increase in uric acid production which, in turn, results in a lowering of nitric oxide in the body [43,44]. Other hypotheses behind high SSB intake being implicated in hypertension involve decreased sodium excretion, activation of the sympathetic nervous system [45,46], or an increased sodium concentration in the body through increased gut absorption [47].…”

Section: Discussionmentioning

confidence: 99%

Relationship between Nutrition and Alcohol Consumption with Blood Pressure: The ESTEBAN Survey

et al. 2019

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Background: Dietary interventions are recommended for the prevention of hypertension. The aim of this study was to evaluate and quantify the relationship between alcohol consumption and the DASH (Dietary Approaches to Stop Hypertension) score with blood pressure (BP) stratified by gender. Methods: Cross-sectional analyses were performed using data from 2105 adults from the ESTEBAN survey, a representative sample of the French population. Pearson correlation analyses were used to assess the correlation between the DASH score and alcohol with BP. Regressions were adjusted by age, treatment, socio-economic level, tobacco, exercise, Body mass index (BMI), and cardiovascular risk factors and diseases. Results: The DASH score was negatively correlated with systolic (SBP) and diastolic BP (DBP) (p < 0.0001). Alcohol was positively associated with increased BP only in men. The worst quintile of the DASH score was associated with an 1.8 mmHg increase in SBP and an 0.6 mmHg increase in SBP compared to the greatest quintile in men and with a 1.5 mmHg increase in SBP and an 0.4 mmHg increase in SBP in women. Male participants in the worst quintile of alcohol consumption showed an increase of 3.0 mmHg in SBP and 0.8 mmHg in DBP compared to those in the greatest quintile. Conclusion: A high DASH score and a reduction in alcohol consumption could be effective nutritional strategies for the prevention of hypertension.

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Hypertension Associated with Fructose and High Salt: Renal and Sympathetic Mechanisms

Cited by 53 publications

References 78 publications

Excessive Fructose Intake Impairs Baroreflex Sensitivity and Led to Elevated Blood Pressure in Rats

Excessive Fructose Intake Impairs Baroreflex Sensitivity and Led to Elevated Blood Pressure in Rats

High-salt diet decreases mechanical thresholds in mice that is mediated by a CCR2-dependent mechanism

Relationship between Nutrition and Alcohol Consumption with Blood Pressure: The ESTEBAN Survey

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