Urinary excretion of dihydroxyphenylalanine and dopamine during alterations of dietary salt intake in humans

1989 ◽  
Vol 76 (5) ◽  
pp. 517-522 ◽  
Author(s):  
David S. Goldstein ◽  
Robin Stull ◽  
Graeme Eisenhofer ◽  
John R. Gill
Keyword(s):  
Urinary Excretion ◽  
Salt Intake ◽  
Sodium Intake ◽  
Sodium Balance ◽  
Dietary Salt ◽  
Proximal Tubular Cells ◽  
Salt Loading ◽  
Dietary Salt Intake ◽  
Tubular Cells ◽  
Proximal Tubular

1. Urinary excretion of dopamine (DA) increases during dietary salt loading. The majority of urinary DA is derived from circulating dihydroxyphenylalanine (dopa). Whether the increase in urinary DA excretion during salt loading results from increased efficiency of uptake of dopa by proximal tubular cells of the kidney, facilitation of intracellular conversion of dopa to DA, or increased delivery of dopa to tubular uptake sites, has been unknown. 2. In 10 inpatient normal volunteers on a constant diet, daily excretion of dopa and DA was assessed during normal sodium intake (109 mmol/day) for 1 week, low sodium intake (9 mmol/day) for 1 week and high sodium intake (249 mmol/day) for 1 week. 3. Urinary DA excretion exceeded urinary dopa excretion by about tenfold, and the excretion of both DA and dopa increased by about twofold between the low and high salt diets, with similar proportionate changes. Plasma dopa was unchanged by dietary salt manipulation. 4. The results indicate that increases in urinary DA excretion during dietary salt loading can be accounted for by increased delivery of dopa to sites of uptake by proximal tubular cells. Since dopa is released into the bloodstream by sympathetic nerve endings and by the brain, and since interference with decarboxylation of dopa attenuates natriuretic responses, dopa may function indirectly as a neurohormone involved in homoeostatic regulation of sodium balance.

Immunoreactive Substance P in Human Plasma: Response to Changes in Posture and Sodium Balance

1980 ◽  
Vol 59 (1) ◽  
pp. 75-77 ◽  
Author(s):  
H. J. Kramer ◽  
R. Düsing ◽  
H. Stelkens ◽  
R. Heinrich ◽  
J. Kipnowski ◽  
...  
Keyword(s):  
Substance P ◽  
Salt Intake ◽  
Sodium Intake ◽  
Plasma Concentrations ◽  
Mean Value ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Dietary Salt ◽  
Dietary Salt Intake ◽  
High Sodium

1. In healthy volunteers plasma concentrations of immunoreactive substance P were measured in response to changes in posture and dietary salt intake. 2. In 14 subjects plasma immunoreactive substance P was 168 ± 31 pmol/l when subjects were supine and 401 ± 51 pmol/l (P < 0.001) when they were ambulant. 3. Measurement of supine plasma immunoreactive substance P at 6 h intervals gave a mean value of 240 ± 39 pmol/l at 14.00 hours and a lowest value of 76 ± 9 pmol/l at 02.00 hours. 4. In eight healthy subjects plasma immunoreactive substance P rose only slightly from 169 ± 41 pmol/l, on a sodium intake ad lib., to 244 ± 45 pmol/l by day 4 of dietary sodium restriction (35 mmol/day) and significantly fell to 51 ± 20 pmol/l (P < 0.001) by day 4 of high sodium intake (350 mmol/day). 5. Although exogenous substance P was shown to be natriuretic in dog and rat, the present results do not favour a role of endogenous substance P as a circulating natriuretic factor in man.

Effects of changes in dietary sodium intake on aortic sodium pump activity in the rat

1987 ◽  
Vol 72 (1) ◽  
pp. 143-146 ◽  
Author(s):  
Richard Bradlaugh ◽  
Robert F. Bing ◽  
John D. Swales ◽  
Herbert Thurston
Keyword(s):  
Smooth Muscle ◽  
Sodium Pump ◽  
Salt Intake ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Dietary Salt ◽  
Salt Loading ◽  
Sodium Efflux ◽  
Salt Restriction ◽  
Dietary Salt Intake

1. Aortic smooth muscle sodium efflux was studied in normal rats undergoing salt restriction or salt loading. 2. Sodium efflux rate constant was not changed by salt loading but fell significantly with salt restriction. This change was not associated with a fall in blood pressure. 3. These studies show that smooth muscle sodium transport can be influenced by dietary salt intake but do not support the concept that salt loading leads to the inhibition of the vascular smooth muscle sodium pump.

scholarly journals Genetically, dietary sodium intake is causally associated with salt-sensitive hypertension risk in a community-based cohort study: a Mendelian randomization approach

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J.R Choi
Keyword(s):  
Mendelian Randomization ◽  
Salt Intake ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Funding Source ◽  
Dietary Salt ◽  
Community Based ◽  
Dietary Salt Intake ◽  
Hypertension Risk ◽  
Salt Sensitive Hypertension

Abstract   Excessive dietary salt intake is associated with an increased risk of hypertension. Salt sensitivity, i.e., an elevation in blood pressure in response to high dietary salt intake, has been associated with a high risk of cardiovascular disease and mortality. We investigated whether a causal association exists between dietary sodium intake and hypertension risk using Mendelian randomization (MR). We performed an MR study using data from a large genome-wide association study comprising 15,034 Korean adults in a community-based cohort study. A total of 1,282 candidate single nucleotide polymorphisms associated with dietary sodium intake, such as rs2960306, rs4343, and rs1937671, were selected as instrumental variables. The inverse variance weighted method was used to assess the evidence for causality. Higher dietary sodium intake was associated with salt-sensitive hypertension risk. The variants of SLC8E1 rs2241543 and ADD1 rs16843589 were strongly associated with increased blood pressure. In the logistic regression model, after adjusting for age, gender, smoking, drinking, exercise, and body mass index, the GRK4 rs2960306TT genotype was inversely associated with hypertension risk (OR = 0.356, 95% CI = 0.236–0.476). However, the 2350GG genotype (ACE rs4343) exhibited a 2.11-fold increased hypertension risk (OR = 2.114, 95% CI = 2.004–2.224) relative to carriers of the 2350AA genotype, after adjusting for confounders. MR analysis revealed that the odds ratio for hypertension per 1 mg/day increment of dietary sodium intake was 2.24 in participants with the PRKG1 rs12414562 AA genotype. Our findings suggest that dietary sodium intake may be causally associated with hypertension risk. Funding Acknowledgement Type of funding source: Public Institution(s). Main funding source(s): This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF), funded by the Ministry of Education (2017R1D1A3B03034119, 2014M3C9A3064552), and the KRIBB Initiative program. This research was also supported by the Medical Research Center Program (2017R1A5A2015369). This work was supported (in part) by the Yonsei University Research Fund 2017. Bioresources for this study were provided by the National Biobank of Korea and the Centers for Disease Control and Prevention, Republic of Korea (2017-009).

scholarly journals Salt and Health: Survey on Knowledge and Salt Intake Related Behaviour in Italy

Nutrients ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 279 ◽  
Author(s):  
Paola Iaccarino Idelson ◽  
Lanfranco D’Elia ◽  
Giulia Cairella ◽  
Paola Sabino ◽  
Luca Scalfi ◽  
...  
Keyword(s):  
Online Survey ◽  
Social Inequalities ◽  
Dietary Habits ◽  
Salt Intake ◽  
Negative Impact ◽  
Sodium Intake ◽  
Italian Population ◽  
Dietary Salt ◽  
Dietary Salt Intake ◽  
Level Of Knowledge

Background and aim: Excess sodium intake is a recognised causal factor of hypertension and its cardiovascular complications; there is however a lack of practical instruments to assess and monitor the level of knowledge and behaviour about dietary salt intake and to relate these factors to the population general dietary habits. Methods and Results: A self-administered questionnaire was developed to assess the salt and health related knowledge and behaviour of the Italian population through an online survey. A sample of 11,618 Italian participants completed the questionnaire. The degree of knowledge and the reported behaviour about salt intake were both found to be related to age, gender, home region, level of education and occupation. There was a significant interrelation between salt knowledge and behaviour and both were significantly and directly related to the degree of adherence to a Mediterranean-like dietary pattern. A hierarchical evaluation was also made of the relevance of any single question to the overall assessment of knowledge and behaviour about salt intake. Conclusions: The study population overall appeared to have a decent level of knowledge about salt, but a less satisfactory behaviour. Our findings point to social inequalities and young age as the main factors having a negative impact on knowledge and behaviour about salt intake as part of generally inadequate dietary habits. The degrees of knowledge and behaviour were significantly and directly interrelated, confirming that improving knowledge is a key step for behavioural changes, and suggesting that educational campaigns are crucial for the implementation of good practices in nutrition.

Osmoregulatory control of renal sodium excretion after sodium loading in humans

1998 ◽  
Vol 275 (6) ◽  
pp. R1833-R1842 ◽  
Author(s):  
Lars Juel Andersen ◽  
Peter Norsk ◽  
Lars Bo Johansen ◽  
Poul Christensen ◽  
Thomas Engstrøm ◽  
...  
Keyword(s):  
Central Venous Pressure ◽  
Sodium Excretion ◽  
Salt Intake ◽  
Sodium Intake ◽  
Venous Pressure ◽  
Sodium Balance ◽  
Plasma Sodium ◽  
Central Venous ◽  
Salt Loading ◽  
Significant Difference

The hypothesis that renal sodium handling is controlled by changes in plasma sodium concentration was tested in seated volunteers. A standard salt load (3.08 mmol/kg body wt over 120 min) was administered as 0.9% saline (Isot) or as 5% saline (Hypr) after 4 days of constant sodium intake of 75 (LoNa+) or 300 mmol/day (HiNa+). Hypr increased plasma sodium by ∼4 mmol/l but increased plasma volume and central venous pressure significantly less than Isot irrespective of diet. After LoNa+, Hypr induced a smaller increase in sodium excretion than Isot (48 ± 8 vs. 110 ± 17 μmol/min). However, after HiNa+the corresponding natriureses were identical (135 ± 33 vs. 139 ± 39 μmol/min), despite significant difference between the increases in central venous pressure. Decreases in plasma ANG II concentrations of 23–52% were inversely related to sodium excretion. Mean arterial pressure, plasma oxytocin and atrial natriuretic peptide concentrations, and urinary excretion rates of endothelin-1 and urodilatin remained unchanged. The results indicate that an increase in plasma sodium may contribute to the natriuresis of salt loading when salt intake is high, supporting the hypothesis that osmostimulated natriuresis is dependent on sodium balance in normal seated humans.

scholarly journals Dietary salt induces transcription of the prostaglandin transporter gene in renal collecting ducts

2008 ◽  
Vol 295 (3) ◽  
pp. F765-F771 ◽  
Author(s):  
Yuling Chi ◽  
Michael L. Pucci ◽  
Victor L. Schuster
Keyword(s):  
Salt Intake ◽  
Collecting Duct ◽  
Prostaglandin E ◽  
Mrna Levels ◽  
Dietary Salt ◽  
Water Excretion ◽  
Salt Loading ◽  
Dietary Salt Intake ◽  
High Sodium ◽  
Transgenic Mouse Line

Prostaglandin E2 (PGE2) plays an important role in maintaining body fluid homeostasis by activating its receptors on the renal collecting duct (CD) to stimulate renal Na+ and water excretion. The PG carrier prostaglandin transporter (PGT) is expressed on the CD apical membrane, where it mediates PG reuptake as part of the termination of autocrine PG signaling. Here we tested the hypothesis that dietary salt loading regulates PGT gene transcription in renal CDs. We placed green fluorescence protein (GFP) under control of 3.3 kb of the mouse PGT promoter and injected this construct into the pronuclei of fertilized FVB mouse eggs. Four of thirty-eight offspring were GFP positive by genotyping. We extensively characterized one (no. 29) PGT-GFP transgenic mouse line. On microscopic examination, GFP was expressed in CDs as determined by their expression of aquaporin-2. We fed mice a low (0.03% NaCl)-, normal (0.3% NaCl)-, or high-salt (3% NaCl) diet for 2 wk and quantified CD GFP expression. The average number of GFP-positive CD cells per microscopic section varied directly with dietary salt intake. Compared with mice on the control (0.3% sodium) diet, mice on a low-sodium (0.03%) diet had reduced numbers of GFP-positive cells (71% of control, P < 0.001), whereas mice on a high-sodium (3%) diet had increased numbers of GFP-positive cells (139% of control, P < 0.001). This increase in apparent CD PGT transcription resulted in a 51–55% increase ( P < 0.001) in whole kidney PGT mRNA levels as determined by real-time PCR. The regulation of PG signal termination via reuptake represents a new pathway for controlling renal Na+ balance.

A Paradoxical Fall in Urine Dopamine Output When Patients with Essential Hypertension Are Given Added Dietary Salt

1984 ◽  
Vol 67 (1) ◽  
pp. 83-88 ◽  
Author(s):  
J. N. Harvey ◽  
I. F. Casson ◽  
A. D. Clayden ◽  
G. F. Cope ◽  
C. M. Perkins ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Sodium Intake ◽  
Statistical Significance ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Control Group ◽  
Dietary Salt ◽  
Salt Loading ◽  
Hypertensive Patients ◽  
Renal Sodium Handling

1. The effect of dietary sodium on the urine dopamine excretion of eight hypertensive patients and six matched controls was studied under metabolic balance conditions over a 2 week period during which dietary sodium intake was increased from 20 to 220 mmol/day. 2. The control group showed the expected increase in dopamine excretion in response to sodium but the hypertensive patients showed an initial fall followed by a return to baseline values. 3. Neither group showed a rise in blood pressure but the hypertensive patients showed a greater weight gain on salt loading, although this change was not significant. The cumulative sodium balance was greater and more prolonged in the hypertensive patients, although this difference also did not attain statistical significance. 4. This defect in dopamine mobilization may be important in relation to renal sodium handling by patients with essential hypertension.

Renal denervation chronically lowers arterial pressure independent of dietary sodium intake in normal rats

2003 ◽  
Vol 284 (6) ◽  
pp. H2302-H2310 ◽  
Author(s):  
Frédéric Jacob ◽  
Pilar Ariza ◽  
John W. Osborn
Keyword(s):  
Arterial Pressure ◽  
Salt Intake ◽  
Sodium Intake ◽  
Recovery Period ◽  
Control Period ◽  
Dietary Sodium ◽  
Renal Nerves ◽  
Dietary Salt ◽  
Dietary Salt Intake ◽  
High Salt Intake

The present study was designed to test the hypothesis that renal nerves chronically modulate arterial pressure (AP) under basal conditions and during changes in dietary salt intake. To test this hypothesis, continuous telemetric recording of AP in intact (sham) and renal denervated (RDNX) Sprague-Dawley rats was performed and the effect of increasing and decreasing dietary salt intake on AP was determined. In protocol 1, 24-h AP, sodium, and water balances were measured in RDNX ( n = 11) and sham ( n = 9) rats during 5 days of normal (0.4% NaCl) and 10 days of high (4.0% NaCl) salt intake, followed by a 3-day recovery period (0.4% NaCl). Protocol 2 was similar with the exception that salt intake was decreased to 0.04% NaCl for 10 days after the 5-day period of normal salt (0.04% NaCl) intake (RDNX; n = 6, sham; n = 5). In protocol 1, AP was lower in RDNX (91 ± 1 mmHg) compared with sham (101 ± 2 mmHg) rats during the 5-day 0.4% NaCl control period. During the 10 days of high salt intake, AP increased <5 mmHg in both groups so that the difference between sham and RDNX rats remained constant. In protocol 2, AP was also lower in RDNX (93 ± 2 mmHg) compared with sham (105 ± 4 mmHg) rats during the 5-day 0.4% NaCl control period, and AP did not change in response to 10 days of a low-salt diet in either group. Overall, there were no between-group differences in sodium or water balance in either protocol. We conclude that renal nerves support basal levels of AP, irrespective of dietary sodium intake in normal rats.

scholarly journals Association of Single Nucleotide Polymorphisms in Salt Taste Receptor Genes With Dietary Salt Intake and Blood Pressure Among Iranian Adults Population

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 945-945
Author(s):  
Noushin Mohammadifard ◽  
Mojgan Gharipour ◽  
Faezeh Moazeni
Keyword(s):  
Blood Pressure ◽  
Salt Intake ◽  
Sodium Intake ◽  
Taste Receptors ◽  
Urine Collection ◽  
Nucleotide Polymorphisms ◽  
Dietary Salt ◽  
Single Nucleotide ◽  
Dietary Salt Intake ◽  
Salt Taste

Abstract Objectives So far, few researches has examined how genetic variation in salt taste receptors affects food intake in Iranian population. Thus, in this study, we aimed to investigate associations of single nucleotide polymorphisms (SNPs) in salt taste receptors genes with dietary salt intake and blood pressure. Methods This cross-sectional study was carried out among 116 randomly selected adults aged 18 years and over in Isfahan city, Iran. Subjects with diabetes insipidus, renal insufficiency, a special dietary regimen, fasting or menstruating on the day of sampling, using diuretics and oral contraceptives or pregnant and lactating women as well as participants who had incomplete 24-h urine collection were excluded. A 24-h urine collection and blood pressure measurement were done. Whole blood was collected to extract DNA and measure SNP rs239345 in the ENaC and rs224534, rs4790151 and rs8065080 in the TRPV1 gene. Results Homozygous carriers of the T allele for rs239345 were found to consume significantly more sodium (4414.7 ± 1943.8 mg/day) compared to the AA genotype (3887.4 ± 1709.1 mg/day). Further, they also had higher diastolic blood pressure compared to subjects with the AA genotype (81.3 ± 9.7 vs. 75.3 ± 8.3 mmHg). Compared to subjects with the CC genotype, those with homozygous carriers of the T allele for rs8065080 in the TRPV1 had higher sodium intake (3592.6 ± 1645.2 mg/day vs. 4604.2 ± 2013.5 mg/day) and systolic blood pressure (118.1 ± 11.3 mmHg vs. 123.4 ± 11.5 mmHg). No differences were found in dietary sodium intake and blood pressure with the rs224534 and rs4790151 SNPs. Conclusions These findings suggest that genetic variation in the ENaC and TRPV1 genes may contribute to inter-individual differences in salt intake and blood pressure. Funding Sources The National Institute for Medical Research Development (NIMAD) was funded this study via grant number of 977,549.

Clearance of endogenous lithium in humans: altered dietary salt intake and comparison with exogenous lithium clearance

1995 ◽  
Vol 268 (4) ◽  
pp. F718-F722 ◽  
Author(s):  
E. Folkerd ◽  
D. R. Singer ◽  
F. P. Cappuccio ◽  
N. D. Markandu ◽  
B. Sampson ◽  
...  
Keyword(s):  
Salt Intake ◽  
Sodium Intake ◽  
Lithium Concentration ◽  
Fractional Excretion ◽  
Dietary Sodium ◽  
Lithium Clearance ◽  
Dietary Salt ◽  
Renal Handling ◽  
Dietary Salt Intake ◽  
High Sodium

We compared endogenous with exogenous lithium clearance (CLi) and studied the effects of dietary salt intake on endogenous CLi in healthy volunteers. Lithium was detectable within a narrow fourfold range in serum and in urine in all 25 subjects studied [serum (n = 25), mean 0.27 +/- 0.02 mumol/l, range 0.13-0.55 mumol/l; urine (n = 20), range 1.49–7.32, mean 4.09 +/- 0.36 mumol/24 h]. Mean clearance and fractional excretion of endogenous lithium were lower (15.2 +/- 2.0 ml/min and 16.4 +/- 2.1%, respectively) compared with results obtained using the exogenous CLi technique (25.5 +/- 1.7 ml/min and 27.9 +/- 2.1%; P < 0.01 and P < 0.05, respectively; n = 17). In a separate group of six normal subjects, absolute (8.7 +/- 2.9 vs. 20.7 +/- 3.8 ml/min) and fractional excretion of lithium (8.3 +/- 2.9 vs. 18.0 +/- 5.1%) were significantly lower on 5 days of low (31 +/- 10 mmol/day) vs. high sodium intake (357 +/- 78 mmol/day; P < 0.05). Use of endogenous CLi precludes the need for lithium tablets. This could be a particular advantage in population studies and permits serial measurement of CLi on different days. Our results show that it is important to take dietary sodium intake into account in studies of endogenous CLi. Lower values for endogenous compared with exogenous CLi could reflect differences in renal handling depending on the plasma lithium concentration. This clearly requires further study.

Sign in / Sign up

Export Citation Format

Share Document