Abstract MP22: Dietary Salt Restriction And High Salt Intake Exaggerate Sympathetic Reflexes And Sensitize Central Autonomic Networks: Potential Mechanisms Of The J-shaped Curve

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Sean D Stocker ◽  
Megan M Wenner ◽  
William B Farquhar
Keyword(s):  
Blood Pressure ◽  
Salt Intake ◽  
Cardiovascular Responses ◽  
Cardiovascular Morbidity ◽  
High Salt ◽  
Dietary Salt ◽  
Salt Restriction ◽  
Salt Diet ◽  
Dietary Salt Intake ◽  
Autonomic Networks

Observational cohort studies suggest that severe salt restriction increases cardiovascular morbidity/mortality, and the relationship between cardiovascular morbidity and dietary salt intake resembles a J-shaped curve. A high salt diet exaggerates sympathetic nerve activity (SNA) and arterial blood pressure (ABP) responses to several cardiovascular reflexes in salt-resistant animals. This study assessed whether salt restriction also exaggerates cardiovascular reflex responses and sensitizes central autonomic networks. To test this hypothesis, male Sprague-Dawley rats were fed low (0.01% NaCl), normal (0.1% NaCl), and high (4.0% NaCl) salt diet for 14-21 days. Baseline mean ABP was not different across groups (low: 104±4, normal: 107±4, high: 107±4mmHg). Activation of sciatic afferents (1ms pulse, 500uA, 5s duration, 2-20Hz) produced significantly greater increases in renal SNA (5Hz; low: 196±12, normal: 136±9, high: 177±8%, n=8, P<0.05) and ABP (5Hz; low: 29±3, normal: 16±1, high: 24±2 mmHg, n=8, P<0.05) of rats fed low and high versus normal NaCl diets. Activation of the aortic depressor nerve (2ms pulse, 500uA, 15s duration, 2-20Hz) produced significantly greater decreases in renal SNA (5Hz; low: -55±9, normal: -34±8, high: -63±13%, n=7-8, P<0.05) and ABP (5Hz; low: -31±3, normal: -15±5, high: -32±5 mmHg, n=7-8, P<0.05) of rats fed low and high versus normal NaCl diets. To test whether dietary salt intake sensitized central sympathetic circuits, microinjection of L-glutamate (0.1-1nmol, 30nL) in the rostral ventrolateral medulla produced significantly greater increases in renal SNA (0.1nmol; low: 212±15, normal: 149±8, high: 183±17%, n=7-8, P<0.05) and ABP (0.1Hz; low: 20±2, normal: 12±2, high: 22±2 mmHg, n=7-8, P<0.05) of rats fed low and high versus normal NaCl diets. Finally, rats fed low or high NaCl versus normal NaCl diets displayed exaggerated cardiovascular responses to cage switch or mild restraint and increased 24-h blood pressure variability. The present findings show that severe salt restriction and excess dietary salt intake exaggerate sympathetic and cardiovascular responses, and may be explained by a parallel change in the sensitivity of central autonomic networks to resemble a J-shaped curve.

scholarly journals High Dietary Salt Intake Exacerbates Helicobacter pylori-Induced Gastric Carcinogenesis

2013 ◽  
Vol 81 (6) ◽  
pp. 2258-2267 ◽  
Author(s):  
Jennifer A. Gaddy ◽  
Jana N. Radin ◽  
John T. Loh ◽  
Feng Zhang ◽  
M. Kay Washington ◽  
...  
Keyword(s):  
Mutant Strain ◽  
Salt Intake ◽  
High Salt ◽  
Dietary Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Content Type ◽  
Dietary Salt Intake ◽  
Regular Diet ◽  
H Pylori

ABSTRACTPersistent colonization of the human stomach withHelicobacter pyloriis a risk factor for gastric adenocarcinoma, andH. pylori-induced carcinogenesis is dependent on the actions of a bacterial oncoprotein known as CagA. Epidemiological studies have shown that high dietary salt intake is also a risk factor for gastric cancer. To investigate the effects of a high-salt diet, we infected Mongolian gerbils with a wild-type (WT)cagA+H. pyloristrain or an isogeniccagAmutant strain and maintained the animals on a regular diet or a high-salt diet. At 4 months postinfection, gastric adenocarcinoma was detected in 100% of the WT-infected/high-salt-diet animals, 58% of WT-infected/regular-diet animals, and none of the animals infected with thecagAmutant strain (P< 0.0001). Among animals infected with the WT strain, those fed a high-salt diet had more severe gastric inflammation, higher gastric pH, increased parietal cell loss, increased gastric expression of interleukin 1β (IL-1β), and decreased gastric expression of hepcidin and hydrogen potassium ATPase (H,K-ATPase) compared to those on a regular diet. Previous studies have detected upregulation of CagA synthesis in response to increased salt concentrations in the bacterial culture medium, and, concordant with thein vitroresults, we detected increasedcagAtranscriptionin vivoin animals fed a high-salt diet compared to those on a regular diet. Animals infected with thecagAmutant strain had low levels of gastric inflammation and did not develop hypochlorhydria. These results indicate that a high-salt diet potentiates the carcinogenic effects ofcagA+H. pyloristrains.

Effects of high-salt diet on CYP450-4A ω-hydroxylase expression and active tone in mesenteric resistance arteries

2005 ◽  
Vol 288 (4) ◽  
pp. H1557-H1565 ◽  
Author(s):  
Jingli Wang ◽  
Richard J. Roman ◽  
John R. Falck ◽  
Lourdes de la Cruz ◽  
Julian H. Lombard
Keyword(s):  
Salt Intake ◽  
High Salt ◽  
Resistance Arteries ◽  
Dietary Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Dietary Salt Intake ◽  
Vasoconstrictor Response ◽  
Cytochrome P 450

This study investigated the role of changes in the expression of the cytochrome P-450 4A (CYP450-4A) enzymes that produce 20-hydroxyeicosatetraenoic acid (20-HETE) in modulating the responses of rat mesenteric resistance arteries to norepinephrine (NE) and reduced Po2 after short-term (3-day) changes in dietary salt intake. The CYP450-4A2, -4A3, and -4A8 isoforms were all detected by RT-PCR in arteries obtained from rats fed a high-salt (HS, 4% NaCl) diet, whereas only the CYP450-4A3 isoform was detected in vessels from rats fed a low-salt (LS, 0.4% NaCl) diet. Expression of the 51-kDa CYP450-4A protein was significantly increased by a HS diet. Inhibiting 20-HETE synthesis with 30 μM N-methylsulfonyl-12,12-dibromododec-11-enamide (DDMS) reduced the vasoconstrictor response to NE in arteries obtained from rats fed either a LS or HS diet, but NE sensitivity after DDMS treatment was significantly lower in vessels from rats on a HS diet. DDMS treatment also restored the vasodilator response to reduced Po2 that was impaired in arteries from rats on a HS diet. These findings suggest that 1) a HS diet increases the expression of CYP450-4A enzymes in the mesenteric vasculature, 2) 20-HETE contributes to the vasoconstrictor response to NE in mesenteric resistance arteries, 3) the contribution of 20-HETE to the vasoconstrictor response to NE is greater in rats fed a HS diet than in rats fed a LS diet, and 4) upregulation of the production of 20-HETE contributes to the impaired dilation of mesenteric resistance arteries in response to hypoxia in rats fed a HS diet.

Effect of Salt Intake and Potassium Supplementation on Urinary Renalase and Serum Dopamine Levels in Chinese Adults

Cardiology ◽  
2015 ◽  
Vol 130 (4) ◽  
pp. 242-248 ◽  
Author(s):  
Yang Wang ◽  
Dan Wang ◽  
Chao Chu ◽  
Jian-Jun Mu ◽  
Man Wang ◽  
...  
Keyword(s):  
Salt Intake ◽  
High Salt ◽  
Dietary Salt ◽  
High Potassium ◽  
High Salt Diet ◽  
Salt Diet ◽  
Dietary Salt Intake ◽  
Potassium Intake ◽  
Potassium Supplementation ◽  
Low Salt

Objective: The aim of our study was to assess the effects of altered salt and potassium intake on urinary renalase and serum dopamine levels in humans. Methods: Forty-two subjects (28-65 years of age) were selected from a rural community of northern China. All subjects were sequentially maintained on a low-salt diet for 7 days (3.0 g/day of NaCl), a high-salt diet for an additional 7 days (18.0 g/day of NaCl), and a high-salt diet with potassium supplementation for a final 7 days (18.0 g/day of NaCl + 4.5 g/day of KCl). Results: Urinary renalase excretions were significantly higher during the high-salt diet intervention than during the low-salt diet. During high-potassium intake, urinary renalase excretions were not significantly different from the high-salt diet, whereas they were significantly higher than the low-salt levels. Serum dopamine levels exhibited similar trends across the interventions. Additionally, a significant positive relationship was observed between the urine renalase and serum dopamine among the different dietary interventions. Also, 24-hour urinary sodium excretion positively correlated with urine renalase and serum dopamine in the whole population. Conclusions: The present study indicates that dietary salt intake and potassium supplementation increase urinary renalase and serum dopamine levels in Chinese subjects.

scholarly journals Modulation of Plasma Sphingosine-1-phosphate Levels via Dietary Salt Intervention in Chinese Adults: An Intervention Trial

2020 ◽  
Author(s):  
Qiong Ma ◽  
Chao Chu ◽  
Yanbo Xue ◽  
Yu Yan ◽  
Jiawen Hu ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Repeated Measures ◽  
Salt Intake ◽  
High Salt ◽  
Dietary Salt ◽  
Chinese Adults ◽  
Salt Diet ◽  
Low Salt ◽  
Sphingosine 1 Phosphate ◽  
Pressure Modulation

Abstract Background: Salt is a crucial factor for blood pressure modulation, especially in salt-sensitive individuals. Sphingosine-1-phosphate (S1P), a pleiotropic bioactive sphingolipid metabolite participating in blood pressure regulation, has recently been identified as a novel lipid diuretic factor. However, the relationships among salt intake, circulating S1P levels, and blood pressure changes in human beings are unknown. Thus, we conducted this intervention trial to explore the effect of dietary salt intake on plasma S1P levels and to examine the relationship between S1P and blood pressure in Chinese adults.Methods: 42 participants (aged 18–65 years) were recruited from a rural community in Shaanxi, China. All participants first maintained their normal diet for 3 days, then sequentially ate a low-sodium diet (3.0 g/day NaCl) for 7 days, followed by a high-sodium diet (18.0 g/day NaCl) for 7 days. We assessed their plasma S1P concentrations on the last day of each intervention phase by liquid chromatography-tandem mass spectrometry. We classified the subjects who demonstrated at least a 10% increase in mean arterial pressure upon transitioning from a low-salt to a high-salt diet as salt-sensitive and the others as salt-resistant. Differences in repeated measures were analyzed by repeated-measures analysis of variance. Results: Plasma S1P levels decreased significantly from the baseline to low-salt diet period and increased from the low-salt to high-salt diet period. We observed this response in both salt-sensitive and salt-resistant individuals. Plasma S1P levels positively correlated with 24-hour urinary sodium excretion, but not 24-hour urinary potassium excretion. In line with plasma S1P level responses to salt intervention, systolic blood pressure (SBP) and mean arterial pressure (MAP) decreased from the baseline to low-salt diet period and increased from the low-salt to high-salt period. SBP positively correlated with plasma S1P and the correlation was stronger in salt-sensitive individuals than that in salt-resistant individuals. Conclusion: Low-salt dietary intervention decreases plasma S1P levels, whereas high-salt intervention reverses this change and S1P levels positively correlated with SBP in Chinese adults. This provides a high-efficiency and low-cost intervention for plasma S1P levels modulation, with implications for salt-induced blood pressure modulation. Trial registration: NCT02915315. Registered 27 September 2016, http://www.clinicaltrials.gov

Regulation ofP-450 4A activity in the glomerulus of the rat

1999 ◽  
Vol 276 (6) ◽  
pp. R1749-R1757 ◽  
Author(s):  
Osamu Ito ◽  
Richard J. Roman
Keyword(s):  
Arachidonic Acid ◽  
Salt Intake ◽  
High Salt ◽  
Dependent Manner ◽  
Hydroxyeicosatetraenoic Acid ◽  
Dietary Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Dietary Salt Intake ◽  
Low Salt

We recently reported that an enzyme of the cytochrome P-450 4A family is expressed in the glomerulus, but there is no evidence that 20-hydroxyeicosatetraenoic acid (20-HETE) can be produced by this tissue. The purpose of present study was to determine whether glomeruli isolated from the kidney of rats can produce 20-HETE and whether the production of this metabolite is regulated by nitric oxide (NO) and dietary salt intake. Isolated glomeruli produced 20-HETE, dihydroxyeicosatrienoic acids, and 12-hydroxyeicosatetraenoic acid (4.13 ± 0.38, 4.20 ± 0.38, and 2.10 ± 0.20 pmol ⋅ min−1⋅ mg protein−1, respectively) when incubated with arachidonic acid (10 μM). The formation of 20-HETE was dependent on the availability of NADPH and the[Formula: see text] of the incubation medium. The formation of 20-HETE was inhibited by NO donors in a concentration-dependent manner. The production of 20-HETE was greater in glomeruli isolated from the kidneys of rats fed a low-salt diet than in kidneys of rats fed a high-salt diet (5.67 ± 0.32 vs. 2.83 ± 0.32 pmol ⋅ min−1⋅ mg protein−1). Immunoblot experiments indicated that the expression of P-450 4A protein in glomeruli from the kidneys of rats fed a low-salt diet was sixfold higher than in kidneys of rats fed a high-salt diet. These results indicate that arachidonic acid is primarily metabolized to 20-HETE and dihydroxyeicosatrienoic acids in glomeruli and that glomerular P-450 activity is modulated by NO and dietary salt intake.

Lithium clearance in man: Effects of dietary salt intake, acute changes in extracellular fluid volume, amiloride and frusemide

1987 ◽  
Vol 73 (6) ◽  
pp. 645-651 ◽  
Author(s):  
J. C. Atherton ◽  
R. Green ◽  
S. Hughes ◽  
V. McFall ◽  
J. A. Sharples ◽  
...  
Keyword(s):  
Volume Expansion ◽  
Salt Intake ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
High Salt ◽  
Extracellular Fluid Volume ◽  
Lithium Clearance ◽  
Dietary Salt ◽  
Salt Diet ◽  
Dietary Salt Intake

1. The effects of amiloride and frusemide on lithium clearance were studied during changes in dietary sodium chloride intake and during infusion of 0.9% NaCl in normal human volunteers. 2. Lithium and fractional lithium clearances were less on the low than on the high salt diet. Values for the medium salt diet were intermediate. Acute extracellular fluid volume expansion with 0.9% NaCl infusion and extracellular fluid volume contraction 3–4 h after intravenous frusemide caused lithium and fractional lithium clearances to increase and decrease respectively. 3. Amiloride caused small changes in lithium and fractional lithium clearances on a low salt diet, but was without effect when salt intake was medium or high. 4. Increases in lithium clearance occurred immediately after frusemide irrespective of dietary salt intake and in subjects infused with 0.9% NaCl. Only in salt-depleted subjects did frusemide cause a substantial increase in fractional lithium clearance. Changes induced under other circumstances were small. 5. It is concluded that the lithium clearance method for assessment of proximal tubule salt and water re-absorption can be used with some degree of confidence in certain circumstances (medium and high salt intake as well as in acute volume expansion) but may not be reliable when dietary salt intake is low.

Links Between Dietary Salt Intake, Renal Salt Handling, Blood Pressure, and Cardiovascular Diseases

2005 ◽  
Vol 85 (2) ◽  
pp. 679-715 ◽  
Author(s):  
Pierre Meneton ◽  
Xavier Jeunemaitre ◽  
Hugh E. de Wardener ◽  
Graham A. Macgregor
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Diseases ◽  
Salt Intake ◽  
Causal Link ◽  
Left Ventricular ◽  
High Salt ◽  
Human Populations ◽  
Dietary Salt ◽  
Dietary Salt Intake ◽  
High Salt Intake

Epidemiological, migration, intervention, and genetic studies in humans and animals provide very strong evidence of a causal link between high salt intake and high blood pressure. The mechanisms by which dietary salt increases arterial pressure are not fully understood, but they seem related to the inability of the kidneys to excrete large amounts of salt. From an evolutionary viewpoint, the human species is adapted to ingest and excrete <1 g of salt per day, at least 10 times less than the average values currently observed in industrialized and urbanized countries. Independent of the rise in blood pressure, dietary salt also increases cardiac left ventricular mass, arterial thickness and stiffness, the incidence of strokes, and the severity of cardiac failure. Thus chronic exposure to a high-salt diet appears to be a major factor involved in the frequent occurrence of hypertension and cardiovascular diseases in human populations.

High dietary salt intake increases carotid blood pressure and wave reflection in normotensive healthy young men

2011 ◽  
Vol 110 (2) ◽  
pp. 468-471 ◽  
Author(s):  
Mirian J. Starmans-Kool ◽  
Alice V. Stanton ◽  
Yun Y. Xu ◽  
Simon A. McG Thom ◽  
Kim H. Parker ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Body Weight ◽  
Wave Reflection ◽  
Salt Intake ◽  
High Salt ◽  
Dietary Salt ◽  
Dietary Salt Intake ◽  
High Salt Intake ◽  
Increased Risk

Dietary salt intake is associated with high brachial blood pressure (BP) and increased risk of cardiovascular disease. We investigated whether changes in dietary salt intake are associated with changes in central BP and wave reflection in healthy volunteers. Ten healthy normotensive male volunteers (22–40 yr) participated in a 6-wk double-blind randomized crossover study to compare a low-dietary salt intake (60–80 mmol sodium/day) with a high-salt intake (low salt intake supplemented with 128 mmol sodium/day) on central BP and wave reflection. Brachial and carotid BP, carotid blood flow velocity, forward (Pf) and backward (Pb) pressure, wave intensity, body weight, and urinary electrolyte excretion were measured at the end of each crossover period. High salt intake significantly increased carotid systolic BP [98 (SD 11) vs. 91 mmHg (SD 13), P < 0.01] and increased wave reflection [ratio of backward to forward pressure (Pb/Pf) 0.13 (SD 0.02) vs. 0.11 (SD 0.03), P = 0.04] despite only small effects on brachial BP [114 (SD 9) vs. 112 mmHg (SD 6), P = 0.1]. Urinary sodium excretion and body weight were also increased following high salt intake. High salt intake disproportionately increases central BP compared with brachial BP as a result of enhanced wave reflection. These effects may contribute to the adverse effect of high dietary salt intake on the risk of cardiovascular disease.

scholarly journals Modulation of Plasma Sphingosine-1-Phosphate Levels via Dietary Salt Intervention in Chinese Adults:an Intervention Trial

2020 ◽  
Author(s):  
Qiong Ma ◽  
Chao Chu ◽  
Yan-bo Xue ◽  
Jia-wen Hu ◽  
Wen-ling Zheng ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Repeated Measures ◽  
Salt Intake ◽  
High Salt ◽  
Dietary Salt ◽  
Chinese Adults ◽  
Salt Diet ◽  
Low Salt ◽  
Sphingosine 1 Phosphate ◽  
Pressure Modulation

Abstract Background: Sphingosine-1-phosphate (S1P), a pleiotropic bioactive sphingolipid metabolite, is involved in various pathophysiological processes,including blood pressure regulation. Salt is a crucial factor for blood pressure modulation,especially in salt-sensitive individuals who may develop earlier, more severe subclinical target organ damage than salt-resistant individuals.However, the relationships among salt intake, circulating S1P levels, and blood pressure changes are unknown. Thus, we conducted this intervention trial to explore the effect of dietary salt intake on plasma S1P levels and examine the relationship between S1P and blood pressure in Chinese adults.Methods:Forty-two participants (aged 18–65 years) were recruited from a rural community in Shaanxi, China. All participants first maintained their normal diet for 3 days, then sequentially ate a low-sodium diet (3.0 g/day NaCl) for 7 days, followed by a high-sodium diet (18.0 g/day NaCl) for 7 days. We assessed their plasma S1P concentrations on the last day of each intervention phase by liquid chromatography–tandem mass spectrometry. We classified the subjects who demonstrated at least a 10% increase in mean arterial pressure upon transitioning from a low-salt to a high-salt diet as salt-sensitive and the others as salt-resistant. Differences in repeated measures were analyzed by repeated-measures analysis of variance. Results:Plasma S1P levels decreased significantly from the baseline to low-salt diet period and increased from the low-salt tohigh-salt diet period. We observed this response in both salt-sensitive and salt-resistant individuals. Plasma S1P levels positively correlated with 24-hour urinary sodium excretion, but not 24-hour urinary potassium excretion. In line with plasma S1P level responses to salt intervention, systolic blood pressure and mean arterial pressure decreased from the baseline to low-salt diet period and increased from the low-salt to high-salt period.Systolic blood pressure positively correlated with plasma S1P; the correlation was stronger in salt-sensitive individuals than in salt-resistant individuals. Conclusion:Low-salt intervention decreased plasma S1P levels, whereas high-salt intervention reversed this changein Chinese adults. This finding provides evidence that salt moderation may be a high-efficiency, low-cost intervention for regulating circulating S1P levels, with implications for salt-induced blood pressure modulation. Trial registration: NCT02915315.Registered 27 September，2016,http://www.clinicaltrials.gov

Sign in / Sign up

Export Citation Format

Share Document