Evidence that the hypothalamus may be a source of a circulating Na+-K+-ATPase inhibitor

1983 ◽  
Vol 98 (2) ◽  
pp. 221-226 ◽  
Author(s):  
J. Alaghband-Zadeh ◽  
S. Fenton ◽  
K. Hancock ◽  
J. Millettt ◽  
H. E. de Wardener
Keyword(s):  
Sodium Intake ◽  
Rat Tissues ◽  
Atpase Inhibitor ◽  
Sodium Potassium ◽  
High Sodium ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Acetone Extracts

Acetone extracts from a variety of rat tissues were tested for their ability to stimulate renal glucose-6-phosphate dehydrogenase (G6PD) activity at 2 min in an in-vitro cytochemical assay which is a marker of the sodium potassium-dependent adenosine triphosphatase (Na+-K+-ATPase) inhibiting activity. Extracts of the hypothalamus were the only ones found to be active in this system. Acetone extract of hypothalamus also inhibited renal Na+-K+-ATPase activity in vitro. The G6PD-stimulating activity from one hypothalamus was about 10000 to 100 000 times greater than that of 1 ml plasma. The G6PD-stimulating activity of hypothalamic extracts from rats which had been on a high sodium intake for 4 weeks were approximately 150 times more active than those obtained from rats which had been on a low sodium diet. The G6PD-stimulating activity of the corresponding plasma was sixfold more active. These findings suggest that a circulating sodium transport inhibitor(s) may be secreted from the hypothalamus.

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.

Alterations in Cerebrospinal Fluid Angiotensin II by Sodium Intake in Patients with Essential Hypertension

1989 ◽  
Vol 77 (4) ◽  
pp. 389-394 ◽  
Author(s):  
Minoru Kawamura ◽  
Yuhei Kawano ◽  
Kaoru Yoshida ◽  
Masahito Imanishi ◽  
Satoshi Akabane ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Essential Hypertension ◽  
Sodium Intake ◽  
Ang Ii ◽  
Sodium Depletion ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium

1. Angiotensin (ANG) levels were measured in the cerebrospinal fluid of 15 patients with essential hypertension on a high sodium diet for 1 week and on a low sodium diet for a further week. ANGs were determined using a system of extraction by Sep-Pak cartridges followed by h.p.l.c. combined with radioimmunoassay. 2. Sodium depletion resulted in increases of ANG II in the cerebrospinal fluid from 1.16 ± 0.38 (sem) to 1.83 ± 0.43 fmol/ml (P < 0.01) and of ANG III from 0.65 ± 0.11 to 0.86 ± 0.15 fmol/ml (P < 0.01). 3. The ANG II level in the cerebrospinal fluid was found to be unchanged and recovery of added ANG II was approximately 90%, even after incubation for 3 h, on both diets. Thus, it is unlikely that ANG II is produced or degraded in the cerebrospinal fluid in vitro. 4. There was no significant correlation between the cerebrospinal fluid and the plasma ANG II concentration on the low sodium diet. 5. These results suggest that the cerebrospinal fluid ANG II level increases with sodium depletion, and that the effect of the level of ANG II on the activity of the angiotensin-forming system in the central nervous system may be assessed by determination of ANG II in the cerebrospinal fluid in patients with essential hypertension.

Dietary sodium intake modulates renal excretory responses to intrarenal angiotensin (1–7) administration in anesthetized rats

2013 ◽  
Vol 304 (3) ◽  
pp. R260-R266 ◽  
Author(s):  
Julie O'Neill ◽  
Alan Corbett ◽  
Edward J. Johns
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Renal Hemodynamic

Angiotensin II at the kidney regulates renal hemodynamic and excretory function, but the actions of an alternative metabolite, angiotensin (1–7), are less clear. This study investigated how manipulation of dietary sodium intake influenced the renal hemodynamic and excretory responses to intrarenal administration of angiotensin (1–7). Renal interstitial infusion of angiotensin (1–7) in anesthetized rats fed a normal salt intake had minimal effects on glomerular filtration rate but caused dose-related increases in urine flow and absolute and fractional sodium excretions ranging from 150 to 200%. In rats maintained for 2 wk on a low-sodium diet angiotensin (1–7) increased glomerular filtration rate by some 45%, but the diuretic and natriuretic responses were enhanced compared with those in rats on a normal sodium intake. By contrast, renal interstitial infusion of angiotensin (1–7) in rats maintained on a high-sodium intake had no effect on glomerular filtration rate, whereas the diuresis and natriuresis was markedly attenuated compared with those in rats fed either a normal or low-sodium diet. Plasma renin and angiotensin (1–7) were highest in the rats on the low-sodium diet and depressed in the rats on a high-sodium diet. These findings demonstrate that the renal hemodynamic and excretory responses to locally administered angiotensin (1–7) is dependent on the level of sodium intake and indirectly on the degree of activation of the renin-angiotensin system. The exact way in which angiotensin (1–7) exerts its effects may be dependent on the prevailing levels of angiotensin II and its receptor expression.

An assay of the capacity of biological fluids to stimulate renal glucose-6-phosphate dehydrogenase activity in vitro as a marker of their ability to inhibit sodium potassium-dependent adenosine triphosphatase activity

1982 ◽  
Vol 94 (1) ◽  
pp. 99-NP ◽  
Author(s):  
S. Fenton ◽  
E. Clarkson ◽  
G. MacGregor ◽  
J. Alaghband-Zadeh ◽  
H. E. de Wardener
Keyword(s):  
Human Plasma ◽  
Adenosine Triphosphatase ◽  
Sodium Intake ◽  
Active Material ◽  
G6pd Activity ◽  
Normal Human Plasma ◽  
Sodium Potassium ◽  
Normal Human ◽  
Glucose 6 Phosphate Dehydrogenase

A highly sensitive cytochemical method for the assay of the ability of plasma and extracts of human urine to stimulate renal glucose-6-phosphate dehydrogenase (G6PD) activity in vitro is described. In the proximal convoluted tubules there was a linear increase of G6PD activity with the logarithm of concentration of a highly purified natriuretic extract from normal human urine (0·384–384 ng active material/l) which was used as a standard. The stimulation of G6PD obtained with dilutions of normal human plasma was parallel to that produced by the standard. The sensitivity of the assay permitted the measurement of as little as 0·384 ng active material/l of the natriuretic extract (0·001 units/ml) and dilutions of 1/10 000 could be detected using normal human plasma. The mean ± s.e.m. index of precision was 0·068± 0·003 (n = 9). It is known that inhibition of sodium potassium-dependent adenosine triphosphatase (Na+-K+-ATPase) is associated with a rise in G6PD activity. We have confirmed this observation by demonstrating that ouabain, a potent inhibitor of Na+ -K+-ATPase, stimulates renal G6PD activity in our assay and that natriuretic extract, human plasma and ouabain stimulated renal G6PD activity in vitro and simultaneously inhibited renal Na+-K+-ATPase activity in vitro. The plasma from 12 normal subjects (five of whom were previously shown to inhibit renal Na+-K+-ATPase activity in vitro in a manner related to sodium intake) stimulated renal G6PD activity in vitro, and this activity was also directly related to sodium intake. It is suggested that the change in the capacity of plasma to stimulate renal G6PD activity in vitro is a marker of the concentration of a circulating sodium transport inhibitor.

scholarly journals Increased renal endothelin formation is associated with sodium retention and increased free water clearance

1998 ◽  
Vol 275 (3) ◽  
pp. H1070-H1077 ◽  
Author(s):  
Pietro Amedeo Modesti ◽  
Ilaria Cecioni ◽  
Angela Migliorini ◽  
Alessandra Naldoni ◽  
Alessandro Costoli ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Free Water ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Sodium Retention ◽  
Free Water Clearance ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Water Clearance

To investigate whether renal endothelin (ET)-1 participates in water and sodium handling, we investigated the influence of different sodium intakes on renal production of ET-1 in eight healthy subjects. The functional relationship with the renin-angiotensin system was also studied. Renal ET-1 formation is affected by sodium intake, because 1 wk of high sodium decreased urinary ET-1 excretion (−34%, P< 0.05), whereas a low-sodium diet increased ET-1 excretion (66%, P < 0.05) and mRNA expression for preproendothelin-1 in epithelial cells of medullary collecting ducts and endothelial cells of the peritubular capillary network. Increased ET-1 renal synthesis was associated with sodium retention and increased free water clearance. Urinary ET-1 excretion changes from normal to low-sodium diet were negatively related to contemporary changes in sodium excretion ( r = 0.97, P < 0.05) and were positively correlated with free water clearance ( r = 0.97, P < 0.05). These correlations were maintained during angiotensin-converting enzyme inhibition, which only partially reduced ET-1 renal excretion. These results indicate that renal ET-1 production is indeed modulated by varying sodium intakes and may exert a role in sodium and water handling.

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.

scholarly journals Sex differences in salt sensitivity to nitric oxide dependent vasodilation in healthy young adults

2012 ◽  
Vol 112 (6) ◽  
pp. 1049-1053 ◽  
Author(s):  
John H. Eisenach ◽  
Leah R. Gullixson ◽  
Susan L. Kost ◽  
Michael J. Joyner ◽  
Stephen T. Turner ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
No Production ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Before And After ◽  
High Sodium Diet

Dietary sodium and blood pressure regulation differs between normotensive men and women, an effect which may involve endothelial production of nitric oxide (NO). Therefore, we tested the hypothesis that differences in the NO component of endothelium-dependent vasodilation between low and high dietary sodium intake depend on sex. For 5 days prior to study, healthy adults consumed a controlled low-sodium diet (10 mmol/day, n = 30, mean age ± SE: 30 ± 1 yr, 16 men) or high-sodium diet (400 mmol/day, n = 36, age 23 ± 1 yr, 13 men). Forearm blood flow (FBF, plethysmography) responses to brachial artery administration of acetylcholine (ACh, 4 μg·100 ml tissue−1·min−1) were measured before and after endothelial NO synthase inhibition with NG-monomethyl-l-arginine (l-NMMA, 50 mg bolus + 1 mg/min infusion). The NO component of endothelium-dependent dilation was calculated as the response to ACh before and after l-NMMA accounting for changes in baseline FBF: [(FBF ACh − FBF baseline) − (FBF AChL-NMMA − FBF baselineL-NMMA)]. This value was 5.7 ± 1.3 and 2.5 ± 0.8 ml·100 ml forearm tissue−1·min−1 for the low- and high-sodium diets, respectively (main effect of sodium, P = 0.019). The sodium effect was larger for the men, with values of 7.9 ± 2.0 and 2.2 ± 1.4 for men vs. 3.1 ± 1.3 and 2.7 ± 1.0 ml·100 ml forearm tissue−1·min−1 for the women ( P = 0.034, sex-by-sodium interaction). We conclude that the NO component of endothelium-dependent vasodilation is altered by dietary sodium intake based on sex, suggesting that endothelial NO production is sensitive to dietary sodium in healthy young men but not women.

scholarly journals High sodium intake increases HCO3− absorption in medullary thick ascending limb through adaptations in basolateral and apical Na+/H+ exchangers

2011 ◽  
Vol 301 (2) ◽  
pp. F334-F343 ◽  
Author(s):  
David W. Good ◽  
Thampi George ◽  
Bruns A. Watts
Keyword(s):  
Absorptive Capacity ◽  
Sodium Intake ◽  
Thick Ascending Limb ◽  
Acid Base Balance ◽  
High Sodium ◽  
High Sodium Intake ◽  
Medullary Thick Ascending Limb ◽  
Nhe1 Activity ◽  
Exchange Activity

A high sodium intake increases the capacity of the medullary thick ascending limb (MTAL) to absorb HCO3−. Here, we examined the role of the apical NHE3 and basolateral NHE1 Na+/H+ exchangers in this adaptation. MTALs from rats drinking H2O or 0.28 M NaCl for 5–7 days were perfused in vitro. High sodium intake increased HCO3− absorption rate by 60%. The increased HCO3− absorptive capacity was mediated by an increase in apical NHE3 activity. Inhibiting basolateral NHE1 with bath amiloride eliminated 60% of the adaptive increase in HCO3− absorption. Thus the majority of the increase in NHE3 activity was dependent on NHE1. A high sodium intake increased basolateral Na+/H+ exchange activity by 89% in association with an increase in NHE1 expression. High sodium intake increased apical Na+/H+ exchange activity by 30% under conditions in which basolateral Na+/H+ exchange was inhibited but did not change NHE3 abundance. These results suggest that high sodium intake increases HCO3− absorptive capacity in the MTAL through 1) an adaptive increase in basolateral NHE1 activity that results secondarily in an increase in apical NHE3 activity; and 2) an adaptive increase in NHE3 activity, independent of NHE1 activity. These studies support a role for NHE1 in the long-term regulation of renal tubule function and suggest that the regulatory interaction whereby NHE1 enhances the activity of NHE3 in the MTAL plays a role in the chronic regulation of HCO3− absorption. The adaptive increases in Na+/H+ exchange activity and HCO3− absorption in the MTAL may play a role in enabling the kidneys to regulate acid-base balance during changes in sodium and volume balance.

Abstract 17541: An Education Intervention Focused on Self-monitoring for Symptom and Sodium Intake Improves Adherence to the Low Sodium Diet and Health Outcome in Patients with Heart Failure

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Eun Kyeung Song ◽  
Debra K Moser ◽  
Seok-Min Kang ◽  
Terry A Lennie
Keyword(s):  
Health Outcomes ◽  
Cox Regression ◽  
Sodium Intake ◽  
Control Group ◽  
Education Intervention ◽  
Self Monitoring ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Patients With Heart Failure

Background: Despite the clinical emphasis on recommending a low sodium diet (LSD), adherence to a LSD remains poor in patients with heart failure (HF). Additional research is needed to determine successful interventions to improve adherence to a LSD and health outcomes. Purpose: To determine the effect of an education intervention on adherence to a LSD and health outcomes. Method: A total of 109 HF patients (age 64±9 years, 29% female) who were non-adherent to LSD, indicating > 3g of 24-hour urinary sodium excretion (24hr UNa) at baseline, were randomly assigned to one of 3 groups: 1) symptom monitoring and restricted 3 gram sodium diet (SMART) group, 2) the telephone monitoring (TM) group, or 3) usual care control group. The SMART group received individualized teaching and guidance of self-monitoring for worsening symptom and sodium intake using symptom and food diary for 4 sessions over 8 weeks. Patients assigned to either of the 2 intervention groups (SMART or TM) received phone calls every 2 weeks over 8 weeks. At 6 months follow-up, adherence to a LSD was assessed using 24hr UNa. Patients were followed for 1 year to determine time to first event of hospitalization or death due to cardiac problems. Repeated measures ANOVA and Cox regression were used to determine the effect of intervention. Results: The SMART group (n=37) showed a significant reduction in sodium intake across time compared to the TM group (n=35) and control group (n=37) (p= .022). In the Cox regression, patients in the SMART group had longer cardiac event-free survival compared to the control group after controlling for age, gender, ejection fraction, angiotensin-converting enzyme inhibitor use, and better blocker use (p=.008). Conclusion: An education intervention focused on self-monitoring for symptom and sodium intake improved adherence to LSD and health outcomes in patients with HF. Helping patients engage in self-monitoring for symptom and sodium intake by themselves can promote better health outcome.

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.

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