Effect of sodium intake on phosphoinositides and inositol trisphosphate response to angiotensin II, K+ and ACTH in rat glomerulosa cells

1989 ◽  
Vol 122 (1) ◽  
pp. 371-377 ◽  
Author(s):  
R. H. Underwood ◽  
A. I. Menachery ◽  
G. H. Williams
Keyword(s):  
Angiotensin Ii ◽  
Sodium Intake ◽  
Time Interval ◽  
Dietary Intakes ◽  
Peak Response ◽  
High Sodium ◽  
Low Sodium ◽  
Phosphatidylinositol 4 ◽  
The Impact ◽  
In Cells

ABSTRACT To assess the impact of sodium intake on the adrenal phosphoinositide system, rats were maintained on a low or normal salt diet for 5 days, and glomerulosa cell preparations (2×105 cells) were stimulated by angiotensin II (AII; 10 nmol/l), potassium (K+; 8·7 mmol/l) or ACTH (0·1 nmol/l) for 0, 2, 4, 6, 12, 15 and 60 s. Levels of phosphatidylinositol (PtdIns), phosphatidylinositol 4-phosphate (PtdIns 4-P), phosphatidylinositol 4,5-bisphosphate (PtdIns 4,5-P2) and inositol 1,4,5-trisphosphate (Ins 1,4,5-P3)+inositol3) + inositol 1,3,4-trisphosphate (Ins 1,3,4-P3) were assayed by a microspectrophotometric procedure. Non-stimulated levels of PtdIns, PtdIns 4-P, PtdIns 4,5-P2 and Ins 1,4,5-P3 (+Ins 1,3,4-P3) (means ± s.e.m.; n = 36) in cells from rats on the low Na+ intake were 580 ± 6·5, 187 ± 2·6, 82 ± 3 and 95 ± 1·2 pmoler incubate respectively, indistinguishable from those observed in rats on a normal Na+ intake, except for the significantly (P<0·025) greater Ptdlns 4,5-P2 level. In response to AII stimulation, all four compounds showed an earlier and greater peak response when cells were obtained from animals on a low rather than a high sodium intake. All values had returned to control levels by 12–15 s, regardless of the level of sodium intake. In contrast, with K+ stimulation there were no differences in the peak response of cells from rats on the two dietary intakes, but there was a shift of the peak to a longer time-interval (6 versus 8 s) in animals maintained on a low sodium intake. In addition, PtdIns 4,5-P2 did not return to control levels in cells obtained from animals on a low sodium intake. However, the most striking differences were observed in response to ACTH. In animals maintained on a normal sodium intake, there were no changes in any of the four compounds. In contrast, there was a sharp increase in all four substances in response to ACTH when the cells were obtained from animals on a low sodium intake, with peak levels occurring at 8 s, similar to that observed with potassium. Thus, changes in the response pattern of the phosphoinositides may mediate the altered adrenal responsiveness to AII and ACTH with sodium restriction. Journal of Endocrinology (1989) 122, 371–377

scholarly journals Remodeling and angiotensin II responses of the uterine arcuate arteries of pregnant rats are altered by low- and high-sodium intake

Reproduction ◽  
2006 ◽  
Vol 131 (2) ◽  
pp. 331-339 ◽  
Author(s):  
Jean St-Louis ◽  
Benoît Sicotte ◽  
Annie Beauséjour ◽  
Michèle Brochu
Keyword(s):  
Angiotensin Ii ◽  
Salt Intake ◽  
Sodium Intake ◽  
High Salt ◽  
Pregnant Rats ◽  
High Sodium ◽  
Sodium Diet ◽  
Uterine Arteries ◽  
Low Sodium Diet ◽  
Low Sodium

Lowering and increasing sodium intake in pregnant rats evoke opposite changes in renin–angiotensin–aldosterone system (RAAS) activity and are associated with alterations of blood volume expansion. As augmented uterine blood flow during gestation is linked to increased circulatory volume, we wanted to determine if low- and high-sodium intakes affect the mechanical properties and angiotensin II (AngII) responses of the uterine vasculature. Non-pregnant and pregnant rats received a normal sodium (0.22% Na+) diet. On the 15th day of gestation some animals were moved to a low-sodium (0.03%) diet, whereas others were given NaCl supplementation as beverage (saline, 0.9% or 1.8%) for 7 days. All rats were killed after 7 days of treatment (eve of parturition). Uterine arcuate arteries (>100 μm) were set up in wire myographs under a tension equivalent to 50 mmHg transmural pressure. The pregnancy-associated increase in diameter of the uterine arteries was significantly attenuated on the low-sodium diet and 1.8% NaCl supplementation. The arcuate arteries of non-pregnant rats on the low-sodium diet showed markedly increased responses to AngII and phenylephrine (Phe). Pregnancy also resulted in heightened responses to AngII and Phe that were significantly reduced for the former agent in rats on the low-sodium diet. Sodium supplementation of non-pregnant rats did not affect the reactivity of the uterine arteries to AngII, but significantly reduced the effect of Phe (1 μmol/l). High salt also significantly diminished the elevated responses to AngII in the arteries of pregnant animals. It was observed that altered sodium intake affects the mechanical and reactive properties of the uterine arcuate arteries more importantly in pregnant than in non-pregnant rats. Low-salt intake similarly affected the reactivity of the uterine arcuate arteries to AngII and Phe, whereas high-salt intake more specifically affected AngII responses. These results showed that perturbations of sodium intake have major impacts on the structure and functions of the uterine arterial circulation, indicating RAAS involvement in uterine vascular remodeling and function during gestation.

Increased Renal Sensitivity to Aldosterone in the Potassium-Loaded Rat

1976 ◽  
Vol 51 (s3) ◽  
pp. 315s-317s
Author(s):  
W. R. Adam ◽  
J. W. Funder
Keyword(s):  
Sodium Intake ◽  
Control Diet ◽  
High Potassium ◽  
High Sodium ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
High K ◽  
And Control

1. The renal response to aldosterone (urinary sodium and potassium excretion) was determined in adrenalectomized rats previously fed either a high potassium diet or a control diet. High K+ rats showed an enhanced response to aldosterone at all doses tested. 2. This enhanced response to aldosterone required the presence of the adrenal glands during the induction period, could be suppressed by a high sodium intake, but could not be induced by a low sodium diet. 3. No difference between high K+ and control rats could be detected in renal mineralocorticoid receptors, assessed by both in vivo and in vitro binding of tritiated aldosterone. 4. The method of the induction, and the mechanism of the enhanced response, remain to be defined.

Abstract P614: Relationship Of Sodium Intake And Stress With Bone Health In Women

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Allison Jasti ◽  
Deborah L Stewart ◽  
Gregory A Harshfield
Keyword(s):  
Bone Health ◽  
Salt Intake ◽  
Sodium Intake ◽  
Target Organ Damage ◽  
African American Adolescents ◽  
Ang Ii ◽  
Mineral Density ◽  
High Sodium ◽  
Low Sodium ◽  
Relationship Of

Background: The skeleton is vital to sodium homeostasis, accounting for 40% of the body’s sodium. Research indicates stress and low sodium intake are independently associated with RAAS activation. In certain populations, stress can induce salt sensitivity, increasing the risk of hypertension and target organ damage, but the association of low versus high sodium intake with bone health is controversial. Purpose: This study sought out the relationship of low sodium and stress-induced RAAS activation with bone health. The tested hypothesis was those with lowest sodium intake would have lower total bone mineral density (TBMD) and content (TBMC) associated with stress-induced increases in angiotensin ii (Ang II) and aldosterone (Aldo). Methods: We compared effect of stress on Ang II, Aldo, TBMD and TMBC in healthy Caucasian and African-American adolescents. Subjects were grouped by quartiles based on sodium intake, assessed by urinary sodium excretion. Results: Due to females, overall significant inverse associations are observed between TBMD, TBMC, Ang II and Aldo in the lowest sodium intake quartile. Post-stress, women in the lowest sodium intake quartile showed that increases in both Ang II and Aldo correspond with lower TMBC and TMBD. There was no significance between Ang II, Aldo, TMBC and TMBD in the three highest quartiles of women nor in any male quartile. Conclusion: These data suggest Ang II and Aldo may reduce TMBC and TMBD in women. Stress-induced increases in Ang II and Aldo, with low sodium intake, may further reduce TBMD and TBMC in women. Ang II inhibition and/or moderated salt intake may be an efficacious prevention or treatment against the development of osteoporosis.

Effect of chloride on renal blood flow in angiotensin II induced hypertension

1991 ◽  
Vol 69 (4) ◽  
pp. 507-511 ◽  
Author(s):  
John C. Passmore ◽  
Agnes E. Jimenez
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Sodium Chloride ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Dietary Sodium ◽  
Maximum Increase ◽  
High Sodium ◽  
Low Sodium ◽  
Chloride Effect

The effect of selective dietary sodium and (or) chloride loading on blood pressure and renal blood flow (RBF) in the rat angiotensin II (AII) model of hypertension was determined. AII (200 ng/min) or saline was infused intraperitoneally. Diets were provided with either high or low concentrations of sodium, chloride or both ions for 22 days. The blood pressure of saline-treated animals was not increased by the high sodium chloride diet. Animals on a high sodium, high chloride diet had a significantly greater increase of blood pressure at 8, 15, 18, and 22 days of AII infusion compared with AII-treated animals on a low sodium, low chloride diet (p < 0.05). Selective dietary loading of either high sodium or chloride in AII-treated rats produced no greater elevation of blood pressure than AII with the low sodium, low chloride diet. Selective high dietary chloride was associated with a lower RBF in AII- and vehicle-treated rats compared with low dietary chloride. The chloride effect on RBF was greater in AII-treated animals. In conclusion, both sodium and chloride are necessary to produce the maximum increase of blood pressure in AII animals. AII enhances the decreased RBF induced by dietary chloride.Key words: angiotensin II, sodium chloride, blood pressure.

scholarly journals Sodium Sensitivity, Sodium Resistance, and Incidence of Hypertension

Hypertension ◽  
2021 ◽  
Author(s):  
Jiang He ◽  
Jian-Feng Huang ◽  
Changwei Li ◽  
Jing Chen ◽  
Xiangfeng Lu ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Experimental Studies ◽  
Dietary Sodium ◽  
Cross Sectional ◽  
Incident Hypertension ◽  
High Sodium ◽  
Sodium Sensitivity ◽  
Sodium Diet ◽  
Low Sodium ◽  
Increased Risk

Cross-sectional studies have reported that high sodium sensitivity is more common among individuals with hypertension. Experimental studies have also reported various animal models with sodium-resistant hypertension. It is unknown, however, whether sodium sensitivity and resistance precede the development of hypertension. We conducted a feeding study, including a 7-day low-sodium diet (1180 mg/day) followed by a 7-day high-sodium diet (7081 mg/day), among 1718 Chinese adults with blood pressure (BP) <140/90 mm Hg. We longitudinally followed them over an average of 7.4 years. Three BP measurements and 24-hour urinary sodium excretion were obtained on each of 3 days during baseline observation, low-sodium and high-sodium interventions, and 2 follow-up studies. Three trajectories of BP responses to dietary sodium intake were identified using latent trajectory analysis. Mean (SD) changes in systolic BP were −13.7 (5.5), −4.9 (3.0), and 2.4 (3.0) mm Hg during the low-sodium intervention and 11.2 (5.3), 4.4 (4.1), and −0.2 (4.1) mm Hg during the high-sodium intervention ( P <0.001 for group differences) in high sodium-sensitive, moderate sodium-sensitive, and sodium-resistant groups, respectively. Compared with individuals with moderate sodium sensitivity, multiple-adjusted odds ratios (95% CIs) for incident hypertension were 1.43 (1.03–1.98) for those with high sodium sensitivity and 1.43 (1.03–1.99) for those with sodium resistance ( P =0.006 for nonlinear trend). Furthermore, a J-shaped association between systolic BP responses to sodium intake and incident hypertension was identified ( P <0.001). Similar results were observed for diastolic BP. Our study indicates that individuals with either high sodium sensitivity or sodium resistance are at an increased risk for developing hypertension.

Abstract MP01: Effect Of The DASH-Sodium Diet On Serum Biomarkers Of Inflammation And Mineral Metabolism

Circulation ◽  
2021 ◽  
Vol 143 (Suppl_1) ◽  
Author(s):  
Valerie K Sullivan ◽  
Lawrence J Appel ◽  
Jesse C Seegmiller ◽  
Casey M Rebholz
Keyword(s):  
Mineral Metabolism ◽  
Sodium Intake ◽  
Random Sequence ◽  
Control Diet ◽  
Fibroblast Growth Factor 23 ◽  
Serum Samples ◽  
Urokinase Plasminogen Activator Receptor ◽  
Dash Diet ◽  
High Sodium ◽  
Low Sodium

Background: The blood pressure-lowering effects of the Dietary Approaches to Stop Hypertension (DASH) dietary pattern and reduced sodium intake are well-established. The effects on other biomarkers related to vascular health are of interest and may assist in explaining cardiovascular benefits of the DASH diet. Objective: We hypothesized that a low-sodium DASH diet improves biomarkers of inflammation [i.e. reduces C-reactive protein (CRP) and soluble urokinase plasminogen activator receptor (suPAR)] and mineral metabolism [phosphorus and fibroblast growth factor-23 (FGF23)]. Methods: We conducted a post hoc analysis of the DASH-Sodium trial using stored frozen serum samples. This controlled feeding study randomized 412 adults to consume either a DASH diet or control diet representative of a typical American diet. Within each arm, participants received three sodium levels (low, intermediate, high) in random sequence, each for 30 days. To maximize contrast, samples collected at the end of the low-sodium DASH (n=198) and high-sodium control (n=194) diets were compared. Between-diet differences in biomarker concentrations were assessed by t-test or Wilcoxon rank sum test for normally distributed and skewed variables, respectively. Results: CRP concentrations did not differ between groups ( P =0.19), but suPAR was higher after the low-sodium DASH diet than the high-sodium control (median, IQR: 2473, 2127-2887 pg/mL vs. 2281, 1929-2679 pg/mL; P =0.003). FGF23 was also higher after the DASH diet (35.9, 26.9-44.8 pg/mL vs. 30.2, 23.5-37.5 pg/mL; P< 0.001). Serum phosphorus was higher after the DASH diet (mean±SEM: 3.5±0.04 mg/dL) versus the control (3.4±0.04 mg/dL; P =0.02). Conclusions: Contrary to our hypothesis, biomarkers of inflammation and mineral metabolism were increased or unchanged by a low-sodium DASH diet compared to a high-sodium control diet. Potential reasons (e.g. short duration of the trial, sodium-specific effects, bioavailable phosphorus-rich dairy intake) require further investigation.

scholarly journals Joint association of urinary sodium and potassium excretion with cardiovascular events and mortality: prospective cohort study

BMJ ◽  
2019 ◽  
pp. l772 ◽  
Author(s):  
Martin O’Donnell ◽  
Andrew Mente ◽  
Sumathy Rangarajan ◽  
Matthew J McQueen ◽  
Neil O’Leary ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Sodium Excretion ◽  
Cardiovascular Events ◽  
Sodium Intake ◽  
Urinary Sodium ◽  
Potassium Excretion ◽  
High Potassium ◽  
High Sodium ◽  
Low Sodium ◽  
Sodium And Potassium

AbstractObjectiveTo evaluate the joint association of sodium and potassium urinary excretion (as surrogate measures of intake) with cardiovascular events and mortality, in the context of current World Health Organization recommendations for daily intake (<2.0 g sodium, >3.5 g potassium) in adults.DesignInternational prospective cohort study.Setting18 high, middle, and low income countries, sampled from urban and rural communities.Participants103 570 people who provided morning fasting urine samples.Main outcome measuresAssociation of estimated 24 hour urinary sodium and potassium excretion (surrogates for intake) with all cause mortality and major cardiovascular events, using multivariable Cox regression. A six category variable for joint sodium and potassium was generated: sodium excretion (low (<3 g/day), moderate (3-5 g/day), and high (>5 g/day) sodium intakes) by potassium excretion (greater/equal or less than median 2.1 g/day).ResultsMean estimated sodium and potassium urinary excretion were 4.93 g/day and 2.12 g/day, respectively. After a median follow-up of 8.2 years, 7884 (6.1%) participants had died or experienced a major cardiovascular event. Increasing urinary sodium excretion was positively associated with increasing potassium excretion (unadjusted r=0.34), and only 0.002% had a concomitant urinary excretion of <2.0 g/day of sodium and >3.5 g/day of potassium. A J-shaped association was observed of sodium excretion and inverse association of potassium excretion with death and cardiovascular events. For joint sodium and potassium excretion categories, the lowest risk of death and cardiovascular events occurred in the group with moderate sodium excretion (3-5 g/day) and higher potassium excretion (21.9% of cohort). Compared with this reference group, the combinations of low potassium with low sodium excretion (hazard ratio 1.23, 1.11 to 1.37; 7.4% of cohort) and low potassium with high sodium excretion (1.21, 1.11 to 1.32; 13.8% of cohort) were associated with the highest risk, followed by low sodium excretion (1.19, 1.02 to 1.38; 3.3% of cohort) and high sodium excretion (1.10, 1.02 to 1.18; 29.6% of cohort) among those with potassium excretion greater than the median. Higher potassium excretion attenuated the increased cardiovascular risk associated with high sodium excretion (P for interaction=0.007).ConclusionsThese findings suggest that the simultaneous target of low sodium intake (<2 g/day) with high potassium intake (>3.5 g/day) is extremely uncommon. Combined moderate sodium intake (3-5 g/day) with high potassium intake is associated with the lowest risk of mortality and cardiovascular events.

Low sodium intake does not impair renal compensation of hypoxia-induced respiratory alkalosis

2002 ◽  
Vol 92 (5) ◽  
pp. 2097-2104 ◽  
Author(s):  
Claudia Höhne ◽  
Willehad Boemke ◽  
Nora Schleyer ◽  
Roland C. Francis ◽  
Martin O. Krebs ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Sodium Intake ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Respiratory Alkalosis ◽  
High Sodium ◽  
Low Sodium ◽  
Oxygen Fraction ◽  
Arterial Blood ◽  
Inspiratory Oxygen

Acute hypoxia causes hyperventilation and respiratory alkalosis, often combined with increased diuresis and sodium, potassium, and bicarbonate excretion. With a low sodium intake, the excretion of the anion bicarbonate may be limited by the lower excretion rate of the cation sodium through activated sodium-retaining mechanisms. This study investigates whether the short-term renal compensation of hypoxia-induced respiratory alkalosis is impaired by a low sodium intake. Nine conscious, tracheotomized dogs were studied twice either on a low-sodium (LS = 0.5 mmol sodium · kg body wt−1 · day−1) or high-sodium (HS = 7.5 mmol sodium · kg body wt−1 · day−1) diet. The dogs breathed spontaneously via a ventilator circuit during the experiments: first hour, normoxia (inspiratory oxygen fraction = 0.21); second to fourth hour, hypoxia (inspiratory oxygen fraction = 0.1). During hypoxia (arterial Po 2 34.4 ± 2.1 Torr), plasma pH increased from 7.37 ± 0.01 to 7.48 ± 0.01 ( P < 0.05) because of hyperventilation (arterial Pco 2 25.6 ± 2.4 Torr). Urinary pH and urinary bicarbonate excretion increased irrespective of the sodium intake. Sodium excretion increased more during HS than during LS, whereas the increase in potassium excretion was comparable in both groups. Thus the quick onset of bicarbonate excretion within the first hour of hypoxia-induced respiratory alkalosis was not impaired by a low sodium intake. The increased sodium excretion during hypoxia seems to be combined with a decrease in plasma aldosterone and angiotensin II in LS as well as in HS dogs. Other factors, e.g., increased mean arterial blood pressure, minute ventilation, and renal blood flow, may have contributed.

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.

The Influence of Sodium Intake on the Pressor Response to Angiotensin II in the Unanaesthetized Rat

1976 ◽  
Vol 50 (4) ◽  
pp. 285-291
Author(s):  
Barbara L. Slack ◽  
J. M. Ledingham
Keyword(s):  
Angiotensin Ii ◽  
Dose Response ◽  
Response Curve ◽  
Dose Response Curve ◽  
Response Curves ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
High Sodium Diet

1. Dose—response curves for the pressor activity of angiotensin II have been determined in unanaesthetized rats receiving diets containing 2·5% (w/w) or 0·007% (w/w) sodium; the different diets were administered in various sequences. 2. In comparison with those from rats receiving a low sodium diet, the dose—response curves were displaced to the left on the high sodium diet, indicating a greater response to angiotensin, and this displacement persisted for a period of approximately 7 days after the diet was changed from high to low sodium. The dose—response curve subsequently shifted to the right when the low sodium diet was maintained for longer. 3. There was a negative correlation between the slope of the dose—response curve and the basal blood pressure in all groups; the correlation was significant in three out of the five different treatment groups. 4. Basal blood pressures were significantly raised in rats on the high sodium diet for 7 days. 5. A number of possible mechanisms have been considered to explain both the parallel shift of the dose—response curve and alteration in its slope. It is concluded that the observed findings are compatible with an action of sodium-loading on the sensitivity of the smooth muscle cell to angiotensin, on the resting of the renin—angiotensin system, on the rate of in-activation of angiotensin and on a change in initial length of the muscle fibre.

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