RAISED PLASMA ANGIOTENSIN II AND ALDOSTERONE DURING DIETARY SODIUM RESTRICTION IN MAN

Liberal or high-sodium (HS) intake, in conjunction with an activated renin–angiotensin–aldosterone system, increases cardiovascular (CV) damage. We tested the hypothesis that sodium intake regulates the type 1 angiotensin II receptor (AT1R), mineralocorticoid receptor (MR), and associated signaling pathways in heart tissue from healthy rodents. HS (1.6% Na+) and low-sodium (LS; 0.02% Na+) rat chow was fed to male healthy Wistar rats (n=7 animals per group). Protein levels were assessed by western blot and immunoprecipitation analysis. Fractionation studies showed that MR, AT1R, caveolin-3 (CAV-3), and CAV-1 were located in both cytoplasmic and membrane fractions. In healthy rats, consumption of an LS versus a HS diet led to decreased cardiac levels of AT1R and MR. Decreased sodium intake was also associated with decreased cardiac levels of CAV-1 and CAV-3, decreased immunoprecipitation of AT1R–CAV-3 and MR–CAV-3 complexes, but increased immunoprecipitation of AT1R/MR complexes. Furthermore, decreased sodium intake was associated with decreased cardiac extracellular signal-regulated kinase (ERK), phosphorylated ERK (pERK), and pERK/ERK ratio; increased cardiac striatin; decreased endothelial nitric oxide synthase (eNOS) and phosphorylated eNOS (peNOS), but increased peNOS/eNOS ratio; and decreased cardiac plasminogen activator inhibitor-1. Dietary sodium restriction has beneficial effects on the cardiac expression of factors associated with CV injury. These changes may play a role in the cardioprotective effects of dietary sodium restriction.

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Decreased insulin sensitivity during dietary sodium restriction is not mediated by effects of angiotensin II on insulin action

Clinical Science ◽

10.1042/cs20020320 ◽

2003 ◽

Vol 105 (2) ◽

pp. 187-194 ◽

Cited By ~ 24

Author(s):

Colin G. PERRY ◽

Tim PALMER ◽

Steven J. CLELAND ◽

Ian J. MORTON ◽

Ian P. SALT ◽

...

Keyword(s):

Insulin Sensitivity ◽

Angiotensin Ii ◽

Insulin Action ◽

Sodium Intake ◽

Second Messengers ◽

Interquartile Range ◽

Dietary Sodium ◽

Sodium Restriction ◽

Double Blind ◽

Dietary Sodium Restriction

We have previously reported that modest dietary sodium restriction, as advocated in management guidelines for diabetes, may reduce insulin sensitivity. It has since been suggested that this effect may be mediated via cross-talk between insulin and angiotensin II (AII)-stimulated intracellular second messengers. In order to assess the effect of 5 days of modest sodium restriction (to <80 mmol/day target sodium intake) on insulin sensitivity, 15 healthy males underwent a double-blind, placebo-controlled, randomized, cross-over euglycaemic hyperinsulinaemic clamp study. One phase was supplemented with sodium tablets and the other with matched placebo. Insulin sensitivity (M) was reduced during dietary sodium restriction [median M value, 10.2 mg/kg per min (interquartile range 9.50–13.85) versus 12.8 mg/kg per min (interquartile range 9.60–14.30), P<0.05]. To elucidate potential mechanisms that may explain this observation, we investigated the effect of AII on insulin action in isolated adipocytes obtained from healthy females. No effect of AII on insulin-mediated glucose transport or suppression of lipolysis was observed. In conclusion, despite the observation that dietary sodium restriction was associated with a median 15% reduction in insulin sensitivity, we found no evidence of a direct effect of AII on insulin action in human adipocytes.

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Influence of Dietary Sodium Restriction on Angiotensin II Receptors in Rat Adrenals*

Endocrinology ◽

10.1210/endo.138.12.5612 ◽

1997 ◽

Vol 138 (12) ◽

pp. 5238-5247 ◽

Cited By ~ 17

Author(s):

Jean-Guy LeHoux ◽

Ian M. Bird ◽

Normand Briere ◽

Denis Martel ◽

Lyne Ducharme

Keyword(s):

Angiotensin Ii ◽

Dietary Sodium ◽

Angiotensin Ii Receptors ◽

Sodium Restriction ◽

Rat Adrenals ◽

Dietary Sodium Restriction

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Faculty Opinions recommendation of Dietary sodium restriction: a neglected therapeutic opportunity in chronic kidney disease.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.718885187.793500395 ◽

2014 ◽

Author(s):

Luis Ruilope ◽

Enrique Morales

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Dietary Sodium ◽

Sodium Restriction ◽

Therapeutic Opportunity ◽

Dietary Sodium Restriction

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The Effects of Short-Term Changes in Sodium Intake on Plasma Marinobufagenin Levels in Patients with Primary Salt-Sensitive and Salt-Insensitive Hypertension

Nutrients ◽

10.3390/nu13051502 ◽

2021 ◽

Vol 13 (5) ◽

pp. 1502

Author(s):

Katarzyna Łabno-Kirszniok ◽

Agata Kujawa-Szewieczek ◽

Andrzej Wiecek ◽

Grzegorz Piecha

Keyword(s):

Blood Pressure ◽

Diastolic Blood Pressure ◽

Sodium Intake ◽

Left Ventricular ◽

Primary Hypertension ◽

Dietary Sodium ◽

Sodium Restriction ◽

Short Term ◽

Salt Loading ◽

Dietary Sodium Restriction

Increased marinobufagenin (MBG) synthesis has been suggested in response to high dietary salt intake. The aim of this study was to determine the effects of short-term changes in sodium intake on plasma MBG levels in patients with primary salt-sensitive and salt-insensitive hypertension. In total, 51 patients with primary hypertension were evaluated during acute sodium restriction and sodium loading. Plasma or serum concentrations of MBG, natriuretic pro-peptides, aldosterone, sodium, potassium, as well as hematocrit (Hct) value, plasma renin activity (PRA) and urinary sodium and potassium excretion were measured. Ambulatory blood pressure monitoring (ABPM) and echocardiography were performed at baseline. In salt-sensitive patients with primary hypertension plasma MBG correlated positively with diastolic blood pressure (ABPM) and serum NT-proANP concentration at baseline and with serum NT-proANP concentration after dietary sodium restriction. In this subgroup plasma MBG concentration decreased during sodium restriction, and a parallel increase of PRA was observed. Acute salt loading further decreased plasma MBG concentration in salt-sensitive subjects in contrast to salt insensitive patients. No correlation was found between plasma MBG concentration and left ventricular mass index. In conclusion, in salt-sensitive hypertensive patients plasma MBG concentration correlates with 24-h diastolic blood pressure and dietary sodium restriction reduces plasma MBG levels. Decreased MBG secretion in response to acute salt loading may play an important role in the pathogenesis of salt sensitivity.

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