Dietary salt enhances benzamil-sensitive component of myogenic constriction in mesenteric arteries

2008 ◽  
Vol 294 (1) ◽  
pp. H409-H420 ◽  
Author(s):  
Nikki L. Jernigan ◽  
Babette LaMarca ◽  
Josh Speed ◽  
Lauren Galmiche ◽  
Joey P. Granger ◽  
...  
Keyword(s):  
Vascular Reactivity ◽  
Salt Intake ◽  
Mesenteric Arteries ◽  
Dietary Sodium ◽  
Epithelial Tissue ◽  
Sprague Dawley ◽  
Resistance Arteries ◽  
Dietary Salt ◽  
Dietary Salt Intake ◽  
And Function

Recent work from our laboratory indicates that epithelial Na+ channel (ENaC) function plays an important role in modulating myogenic vascular reactivity. Increases in dietary sodium are known to affect vascular reactivity. Although previous studies have demonstrated that dietary salt intake regulates ENaC expression and activity in epithelial tissue, the importance of dietary salt on ENaC expression in vascular smooth muscle cells (VSMCs) and its role in myogenic constriction is unknown. Therefore, the goal of the present study was to determine whether dietary salt modulates ENaC expression and function in myogenic vasoconstriction. To accomplish this goal, we examined ENaC expression in freshly dispersed VSMCs and pressure-induced vasoconstrictor responses in isolated mesenteric resistance arteries from normotensive Sprague-Dawley rats fed a normal-salt (NS; 0.4% NaCl) or high-salt (HS; 8% NaCl for 2 wk) diet. VSMCs from the mesenteric arteries of NS-fed animals express α-, β-, and γ-ENaC. The HS diet reduced whole cell α- and γ-ENaC and induced a pronounced translocation of β-ENaC from intracellular regions toward the VSMC membrane (∼336 nm). Associated with this change in expression was a change in the importance of ENaC in pressure-induced constriction. Pressure-induced constriction in NS-fed animals was insensitive to ENaC inhibition with 1 μM benzamil, suggesting that ENaC proteins do not contribute to myogenic constriction in mesenteric arteries under NS intake. In contrast, ENaC inhibition blocked pressure-induced constriction in HS-fed animals. These data suggest that dietary sodium regulates ENaC expression and the quantitative importance of the vascular ENaC signaling pathway contributing to myogenic constriction.

Elevated salt intake impairs dilation of rat skeletal muscle resistance arteries via ANG II suppression

2000 ◽  
Vol 278 (2) ◽  
pp. H500-H506 ◽  
Author(s):  
David S. Weber ◽  
Julian H. Lombard
Keyword(s):  
Salt Intake ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Resistance Arteries ◽  
Dietary Salt ◽  
Short Term ◽  
Dietary Salt Intake ◽  
Sprague Dawley Rats ◽  
Camp And Cgmp ◽  
Prostacyclin Analog

Vasodilator responses were assessed in resistance arteries (100–200 μm) isolated from the gracilis muscle of normotensive rats after changes in dietary salt intake. Sprague-Dawley rats were maintained on either a high-salt (HS) diet (4.0% NaCl) or a low-salt (LS) diet (0.4% NaCl) for 4–8 wk (chronic) or 3 days (short-term) with water ad libitum. One group of short-term HS rats received a continuous intravenous infusion of a low dose (5 ng ⋅ kg− 1 ⋅ min− 1) of ANG II to prevent the ANG II suppression that occurs with HS diet. Short-term and chronic HS diet eliminated arterial dilation in response to ACh and reduced[Formula: see text] (30–40 mmHg) and the stable prostacyclin analog iloprost. ANG II infusion preserved the response to these vasodilator stimuli in short-term HS animals. Dilator responses to sodium nitroprusside and forskolin were unaffected by HS diet. These findings suggest that ANG II suppression during HS diet impairs vascular relaxation mechanisms upstream from the cAMP and cGMP second messenger systems.

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.

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.

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).

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.

Abstract 445: Increased Dietary Salt Intake Enhances Sympathetic and Cardiovascular Responses to Various Stressors

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Sean D Stocker ◽  
Sarah S Simmonds
Keyword(s):  
Salt Intake ◽  
Sympathetic Neurons ◽  
Cardiovascular Responses ◽  
Ventrolateral Medulla ◽  
Cardiovascular Reflexes ◽  
Sprague Dawley ◽  
Dietary Salt ◽  
Dietary Salt Intake ◽  
Intracerebroventricular Infusion ◽  
Arterial Blood

Previous studies indicate that increased dietary salt intake enhances sympathetic nerve activity (SNA) and arterial blood pressure (ABP) responses evoked from sympathetic neurons of the rostral ventrolateral medulla. The present study sought to extend these findings and determine whether dietary salt intake enhances SNA and ABP responses various sympathetic reflexes that depend on RVLM neurotransmission. Male Sprague-Dawley rats were fed 0.1% (n=6-8) or 4.0% (n=6-8) NaCl diets for 14-21 days. Then, animals were anesthetized with Inactin. Electrical stimulation (1-20 Hz, 1 ms pulse, 500 uA) of sciatic afferents produced frequency-dependent changes in SNA and ABP in both groups. However, rats ingesting 4% versus 0.1% NaCl displayed significantly larger increases in lumbar SNA (5Hz: 213±25 vs 146±25%, P<0.05), renal SNA (5Hz: 187±24 vs 120±11%), splanchnic SNA (5Hz: 203±21 vs 136±9%), and mean ABP (5Hz: 28±2 vs 12±2 mmHg). Rats ingesting 4% vs 0.1% NaCl also displayed greater increases in lumbar SNA (24±6 vs 13±2%, P<0.05) and mean ABP (12.1±0.9 vs 8.2±1.3mmHg, P<0.05) during increases in cerebrospinal fluid sodium concentration produced by intracerebroventricular infusion of 1M NaCl (5ul/10min). Lastly, hypercapnia (7% CO2, 33% O2, 63% N2, 60s) produced greater increases in lumbar SNA in rats ingesting 4% versus 0.1% NaCl (24±2% versus 9±3%, respectively; P<0.01). These findings suggest increased dietary salt intake enhances several sympathetic and cardiovascular reflexes.

Abstract 083: Neurons in the Organum Vasculosum of the Lamina Terminalis Contribute to Salt-sensitive Hypertension

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Sean D Stocker
Keyword(s):  
Salt Intake ◽  
Lamina Terminalis ◽  
Sprague Dawley ◽  
Dietary Salt ◽  
Dietary Salt Intake ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
Organum Vasculosum ◽  
Salt Sensitive Hypertension

Excess dietary salt intake raises plasma and cerebrospinal fluid NaCl concentrations to elevate sympathetic nerve activity (SNA) and arterial blood pressure (ABP). Changes in extracellular NaCl concentrations are sensed by neurons in the organum vasculosum of the lamina terminalis (OVLT) - a circumventricular organ that lacks a complete blood-brain barrier. The purpose of the present study was to investigate the hypothesis that salt-sensitive hypertension was mediated, in part, by an elevated activity of OVLT neurons. Dahl-Salt-Sensitive or Sprague-Dawley rats (8-10 weeks) were fed 0.5% or 4.0% NaCl diets for 3-4 weeks. First, in vivo single-unit recordings demonstrate the discharge of OVLT neurons in Dahl-Salt-Sensitive rats was higher after a 4.0% versus 0.5% NaCl diet (4.1±0.4 Hz vs 1.9±0.3 Hz, n=6 per group, P<0.05). OVLT neuronal discharge of Sprague-Dawley rats was not different after a 4.0% or 0.5% NaCl diet (2.1±0.4 Hz vs 1.7±0.3 Hz, n=6-9 per group, P>0.5). In a second set of experiments, injection of hypertonic NaCl (1.0M NaCl, 20nL) into the OVLT produced significantly greater increases in lumbar SNA (131±6% vs 116±3%, n=4 per group, P<0.05) and mean ABP (14±2 vs 8±2 mmHg, n=4 per group, P<0.05) of Dahl-Salt-Sensitive rats fed 4.0% versus 0.5% NaCl respectively. Sprague-Dawley rats fed 4.0% versus 0.5% NaCl exhibited responses of smaller magnitude for both lumbar SNA (115±4 vs 108±3%, n=4 per group, P<0.05) and mean ABP (9±2 vs 6±2 mmHg, n=4 per group, P<0.05). Interestingly, the duration of the response was much longer in Dahl-Salt-Sensitive versus Sprague-Dawley rats (data not shown). Finally, inhibition of neuronal activity by injection of the GABA agonist muscimol (5mM, 20nL) into the OVLT produced a significantly greater fall in lumbar SNA (-25±4% vs -11±3%, n=4 per group, P<0.05) and mean ABP (-19±4 vs -6±2 mmHg, n=4 per group, P<0.05) of Dahl-Salt-Sensitive rats fed 4.0% versus 0.5% NaCl, respectively. Injection of muscimol into the OVLT of Sprague-Dawley rats did not significantly affect SNA or mean ABP. Collectively, these findings suggest a high salt diet increases the activity of OVLT neurons to elevate SNA and ABP in salt-sensitive hypertension.

scholarly journals DIETARY SALT INTAKE: HISTORY, ASSESSMENT, AND BENEFIT IN HYPERTENSIVE TREATMENT

2016 ◽  
pp. 39
Author(s):  
Sunitha Esther Raj ◽  
Lee Mei Tan ◽  
Adyani Md Redzuan
Keyword(s):  
Salt Intake ◽  
Urinary Sodium ◽  
Dietary Sodium ◽  
Dietary Salt ◽  
Dietary Survey ◽  
Pharmacological Management ◽  
Dietary Salt Intake ◽  
Salt Hypertension ◽  
Health Complications ◽  
Improve Health

<p>ABSTRACT<br />Multiple lines of investigation including genetic, epidemiological, and interventional studies have demonstrated consistently a positive relationship<br />between salt intake, blood pressure (BP) increment, and cardiovascular consequences. In addition, it has been documented that excessive salt intake<br />can be attributed to various health complications such as asthma, osteoporosis, obesity, and gastric cancer. On the contrary, a reduction in salt intake<br />has been shown to reduce BP and improve health outcomes, although the evidence is not completely unequivocal. Despite this discrepancy, a lowsodium<br />diet<br />is widely<br />being recommended<br />to<br />all hypertensive<br />patients in<br />particular,<br />as evidence<br />against<br />its efficacy in<br />conjunction with optimum<br />hypertensive<br />treatment<br />is<br />well<br />established.<br />Determination<br />of<br />salt<br />intake<br />among hypertensive<br />patients is important<br />since dietary<br />salt<br />restriction<br />had</p><p>been<br />proven<br />to<br />improve<br />BP control<br />in conjunction with optimum pharmacological management.<br />Various<br />methods<br />have<br />been used to<br />estimate<br />sodium<br />intake<br />includes 24-hrs<br />urinary<br />sodium,<br />overnight<br />urinary sodium,<br />spot<br />urinary sodium/creatinine<br />ratio,<br />and dietary survey<br />methods. Reducing</p><p>population<br />salt<br />intake<br />has been proven<br />to<br />be beneficial, preventing<br />millions<br />of<br />deaths from<br />cardiovascular<br />disease<br />and<br />stroke,<br />and reducing<br />the burden</p><p>on<br />health<br />services.<br />Many<br />individual<br />countries around<br />the globe<br />have<br />already<br />taken<br />action against<br />reducing<br />population<br />salt<br />intake.<br />These strategies</p><p>were<br />either led by<br />government,<br />nongovernment<br />organizations,<br />or industry.<br />Keywords: Dietary sodium, Salt, Hypertension, Sodium measurement, Cost-effectiveness.</p>

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.

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