scholarly journals High Sodium Intake Strengthens the Association between Angiotensinogen T174M Polymorphism and Blood Pressure Levels among Lean Men and Women: a Community-Based Study

2004 ◽  
Vol 27 (1) ◽  
pp. 53-60 ◽  
Author(s):  
Kazumasa YAMAGISHI ◽  
Hiroyasu ISO ◽  
Takeshi TANIGAWA ◽  
Renzhe CUI ◽  
Minako KUDO ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Intake ◽  
Community Based ◽  
Men And Women ◽  
High Sodium ◽  
High Sodium Intake ◽  
T174m Polymorphism

scholarly journals Urinary Sodium and Potassium Levels and Blood Pressure in Population with High Sodium Intake

Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3442
Author(s):  
Da Young Song ◽  
Jiyoung Youn ◽  
Kyunga Kim ◽  
Joohon Sung ◽  
Jung Eun Lee
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Twin Study ◽  
Sodium Intake ◽  
Urinary Sodium ◽  
Creatinine Ratio ◽  
Food Groups ◽  
Men And Women ◽  
High Sodium ◽  
High Sodium Intake

The purpose of this study was to examine the association of urinary sodium-to-creatinine ratio and potassium-to-creatinine ratio with blood pressure in a cross-sectional study comprising Korean adults who participated in the Healthy Twin Study. The participants consisted of 2653 men and women in the Healthy Twin Study aged ≥19 years. Participants’ urinary excretion of sodium, potassium, and creatinine was measured from overnight half-day urine samples. Food intake was assessed using a validated food frequency questionnaire. We examined systolic and diastolic blood pressures according to sodium- or potassium-to-creatinine ratios using the generalized linear model. We determined food groups explaining high urinary sodium- or potassium-to-creatinine ratio using the reduced rank regression and calculated sodium- or potassium-contributing food score. We observed that systolic blood pressure was higher among men and women in the highest quintile of urinary sodium-to-creatinine ratio or sodium-to-potassium ratio than it was in the lowest quintile. Geometric means (95% CIs) of the lowest and the highest quintiles of systolic blood pressure (mmHg) were 113.4 (111.8–115.0) and 115.6 (114.1–117.2; P for trend = 0.02), respectively, for sodium-to-creatinine ratio. The association between urinary sodium-to-creatinine and systolic blood pressure was more pronounced among individuals whose body mass index (BMI) was less than 25 kg/m2 (P for interaction = 0.03). We found that vegetables, kimchi and seaweed intake contributed to high sodium intake and a sodium-contributing food score were associated with increased blood pressure. In our study, we identified the food groups contributing to high sodium intake and found that high urinary sodium levels were associated with increasing blood pressure among Korean adults.

Renal and cardiac oxidative/nitrosative stress in salt-loaded pregnant rat

2007 ◽  
Vol 293 (4) ◽  
pp. R1657-R1665 ◽  
Author(s):  
Annie Beauséjour ◽  
Véronique Houde ◽  
Karine Bibeau ◽  
Rébecca Gaudet ◽  
Jean St-Louis ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Nitrosative Stress ◽  
Gestational Hypertension ◽  
Sodium Intake ◽  
Pregnant Rats ◽  
High Sodium ◽  
High Sodium Intake ◽  
Arterial Blood ◽  
Cardiac Ventricle

Sodium supplementation given for 1 wk to nonpregnant rats induces changes that are adequate to maintain renal and circulatory homeostasis as well as arterial blood pressure. However, in pregnant rats, proteinuria, fetal growth restriction, and placental oxidative stress are observed. Moreover, the decrease in blood pressure and expansion of circulatory volume, normally associated with pregnancy, are prevented by high-sodium intake. We hypothesized that, in these pregnant rats, a loss of the balance between prooxidation and antioxidation, particularly in kidneys and heart, disturbs the normal course of pregnancy and leads to manifestations such as gestational hypertension. We thus investigated the presence of oxidative/nitrosative stress in heart and kidneys following high-sodium intake in pregnant rats. Markers of this stress [8-isoprostaglandin F2α (8-iso-PGF2α) and nitrotyrosine], producer of nitric oxide [nitric oxide synthases (NOSs)], and antioxidants [superoxide dismutase (SOD) and catalase] were measured. Then, molecules (Na+-K+-ATPase and aconitase) or process [apoptosis (Bax and Bcl-2), inflammation (monocyte chemoattractant protein-1, connective tissue growth factor, and TNF-α)] susceptible to free radicals was determined. In kidneys from pregnant rats on 1.8% NaCl-water, NOSs, apoptotic index, and nitrotyrosine expression were increased, whereas Na+-K+-ATPase mRNA and activity were decreased. In the left cardiac ventricle of these rats, heightened nitrotyrosine, 8-iso-PGF2α, and catalase activity together with reduced endothelial NOS protein expression and SOD and aconitase activities were observed. These findings suggest that oxidative/nitrosative stress in kidney and left cardiac ventricle destabilizes the normal course of pregnancy and could lead to gestational hypertension.

High-sodium intake prevents pregnancy-induced decrease of blood pressure in the rat

2003 ◽  
Vol 285 (1) ◽  
pp. H375-H383 ◽  
Author(s):  
Annie Beauséjour ◽  
Karine Auger ◽  
Jean St-Louis ◽  
Michèle Brochu
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Sodium Intake ◽  
Plasma Sodium ◽  
Mrna Levels ◽  
Sprague Dawley ◽  
Pregnant Rats ◽  
High Sodium ◽  
High Sodium Intake ◽  
The Impact

Despite an increase of circulatory volume and of renin-angiotensin-aldosterone system (RAAS) activity, pregnancy is paradoxically accompanied by a decrease in blood pressure. We have reported that the decrease in blood pressure was maintained in pregnant rats despite overactivation of RAAS following reduction in sodium intake. The purpose of this study was to evaluate the impact of the opposite condition, e.g., decreased activation of RAAS during pregnancy in the rat. To do so, 0.9% or 1.8% NaCl in drinking water was given to nonpregnant and pregnant Sprague-Dawley rats for 7 days (last week of gestation). Increased sodium intakes (between 10- and 20-fold) produced reduction of plasma renin activity and aldosterone in both nonpregnant and pregnant rats. Systolic blood pressure was not affected in nonpregnant rats. However, in pregnant rats, 0.9% sodium supplement prevented the decreased blood pressure. Moreover, an increase of systolic blood pressure was obtained in pregnant rats receiving 1.8% NaCl. The 0.9% sodium supplement did not affect plasma and fetal parameters. However, 1.8% NaCl supplement has larger effects during gestation as shown by increased plasma sodium concentration, hematocrit level, negative water balance, proteinuria, and intrauterine growth restriction. With both sodium supplements, decreased AT1 mRNA levels in the kidney and in the placenta were observed. Our results showed that a high-sodium intake prevents the pregnancy-induced decrease of blood pressure in rats. Nonpregnant rats were able to maintain homeostasis but not the pregnant ones in response to sodium load. Furthermore, pregnant rats on a high-sodium intake (1.8% NaCl) showed some physiological responses that resemble manifestations observed in preeclampsia.

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 High Sodium Intake Strengthens the Association of ACE I/D Polymorphism with Blood Pressure in a Community

2007 ◽  
Vol 20 (7) ◽  
pp. 751-757 ◽  
Author(s):  
K YAMAGISHI ◽  
T TANIGAWA ◽  
R CUI ◽  
M TABATA ◽  
A IKEDA ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Intake ◽  
High Sodium ◽  
High Sodium Intake

Sodium restriction can delay the return of hypertension in patients previously well-controlled on drug therapy

1987 ◽  
Vol 65 (8) ◽  
pp. 1752-1755 ◽  
Author(s):  
Trefor Morgan ◽  
Adrianne Anderson
Keyword(s):  
Blood Pressure ◽  
Drug Therapy ◽  
Response Curve ◽  
Sodium Intake ◽  
Reduce Blood Pressure ◽  
Sodium Restriction ◽  
Salt Diet ◽  
Hypertensive Patients ◽  
High Sodium ◽  
High Sodium Intake

Sodium restriction can reduce blood pressure in hypertensive patients. The present study indicates that if hypertension is well controlled then the reemergence of hypertension can be decreased by the use of a reduced sodium intake. The present paper demonstrates that in such patients on a normal salt diet, 90% become hypertensive within 6 months while only 40% of people on a reduced sodium diet become hypertensive. It is proposed that a high sodium intake activates a number of amplifiers that causes a shift of the dose–response curve to sodium to the left and if not prevented or interrupted leads to the development of hypertension.

Effects of Nifedipine during Low, Normal and High Intakes of Sodium in Patients with Essential Hypertension

1982 ◽  
Vol 63 (s8) ◽  
pp. 447s-450s ◽  
Author(s):  
Gloria Valdés ◽  
M. Eugenia Soto ◽  
Hector R. Croxatto ◽  
Teresa Bellolio ◽  
Ramón Corbalán ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Hypotensive Effect ◽  
Sodium Balance ◽  
Hypotensive Action ◽  
High Sodium ◽  
High Sodium Intake ◽  
Low Sodium Diet

1. Nifedipine (20 mg) was given by mouth to seven patients with moderate essential hypertension receiving a low, normal or high sodium intake. The drug produced an important hypotensive effect. Normal sodium intake enhanced the hypotensive action of the drug compared with that during the low and high sodium regimens. Blood pressure remained significantly lower 3 h after drug ingestion. 2. Increases in heart rate and plasma renin activity under all conditions reflected enhanced adrenergic activity. 3. A short-term natriuresis followed nifedipine ingestion in spite of increased aldosterone excretion during the low sodium diet and a decrease in urinary kallikrein during the low and high sodium diets. 4. Nifedipine increased urinary volume only during the high sodium intake. 5. Apart from vasodilatation, nifedipine induces important changes in neurogenic, renal and adrenal mechanisms that regulate blood pressure homoeostasis. Different conditions of sodium balance modulate most of these effects.

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