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

2003 ◽  
Vol 105 (2) ◽  
pp. 187-194 ◽  
Author(s):  
Colin G. PERRY ◽  
Tim PALMER ◽  
Steven J. CLELAND ◽  
Ian J. MORTON ◽  
Ian P. SALT ◽  
...  

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.

2011 ◽  
Vol 211 (1) ◽  
pp. 47-54 ◽  
Author(s):  
Vincent Ricchiuti ◽  
Nathalie Lapointe ◽  
Luminita Pojoga ◽  
Tham Yao ◽  
Loc Tran ◽  
...  

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.


Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1502
Author(s):  
Katarzyna Łabno-Kirszniok ◽  
Agata Kujawa-Szewieczek ◽  
Andrzej Wiecek ◽  
Grzegorz Piecha

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.


1989 ◽  
Vol 256 (6) ◽  
pp. E863-E871 ◽  
Author(s):  
H. Hisa ◽  
Y. H. Chen ◽  
K. J. Radke ◽  
J. L. Izzo ◽  
C. D. Sladek ◽  
...  

These experiments evaluated the contribution of alpha- and beta-adrenergic stimulation to plasma renin activity (PRA) during early and long-term dietary sodium restriction, compared with normal sodium intake. Uninephrectomized conscious dogs with catheters in the aorta, vena cava, and remaining renal artery were studied during normal sodium diet (approximately 70 meq/day), after 2-3 days of low-sodium diet (5-7 meq/day), and after greater than or equal to 2 wk of low-sodium diet. Direct renal arterial (ira) infusion of phenoxybenzamine plus propranolol decreased PRA by similar proportions (39-48%) during all three states of dietary sodium intake. The PRA achieved after adrenergic blockade remained higher (P less than 0.05) during early and long-term sodium restriction than during normal sodium intake. The effect on PRA of ira infusion of propranolol alone was not different from that of phenoxybenzamine plus propranolol during normal or low-sodium diet, and the magnitude of decrease in PRA during low-sodium diet was the same whether propranolol (1 microgram.kg-1.min-1) was infused ira or intravenously. In summary, beta-adrenergic stimulation accounts for similar proportions of PRA during early and long-term dietary sodium restriction and during normal sodium intake. Renal alpha-adrenoceptors appear to play little or no role in control of PRA under these conditions.


The Lancet ◽  
1972 ◽  
Vol 300 (7787) ◽  
pp. 1106-1107 ◽  
Author(s):  
J.J. Brown ◽  
A.F. Lever ◽  
J.J. Morton ◽  
R. Fraser ◽  
D.R. Love ◽  
...  

2016 ◽  
Vol 101 (11) ◽  
pp. 3989-3996 ◽  
Author(s):  
Rene Baudrand ◽  
Francisco J. Guarda ◽  
Jasmine Torrey ◽  
Gordon Williams ◽  
Anand Vaidya

Context: The aldosterone to renin ratio (ARR) is recommended to screen for primary aldosteronism (PA). Objective: To evaluate whether dietary sodium restriction results in misinterpretation of PA screening. Participants: Untreated hypertensives with ARR more than 20 on a high dietary sodium intake (HS) were also evaluated on a low dietary sodium intake (LS) (n = 241). Positive screening for PA was defined as: plasma renin activity (PRA) less than or equal to 1.0 ng/mL · h with serum aldosterone more than or equal to 6 ng/dL. PA was confirmed by a 24-hour urinary aldosterone excretion more than or equal to 12 mcg with urinary sodium more than 200 mmol. Results: Only 33% (79/241) of participants with an ARR more than 20 had a positive PA screen on HS. On LS, 56% (44/79) of these participants no longer met criteria for positive PA screening. When compared with participants with positive PA screening on both diets, participants with a positive screen on HS but negative on LS exhibited a significantly higher PRA on both diets. Remarkably, of the 48/79 participants who had PA confirmed, 52% had negative PA screening on LS. The distinguishing feature of these participants with “discordant” screening results was a larger rise in PRA on LS resulting in normalization of the ARR and higher Caucasian race prevalence. Conclusions: Sodium restriction is recommended in hypertension; however, it can significantly raise PRA, normalize the ARR, and result in false interpretation of PA screening. Milder phenotypes of PA, where PRA is not as suppressed, are most susceptible to dietary sodium influences on renin and ARR. Optimal screening for PA should occur under conditions of HS.


1990 ◽  
Vol 124 (3) ◽  
pp. 507-513 ◽  
Author(s):  
E. A. P. Steegers ◽  
Th. J. Benraad ◽  
H. W. Jongsma ◽  
A. C. I. T. L. Tan ◽  
P. R. Hein

ABSTRACT The effects of dietary sodium restriction and posture on plasma concentrations of atrial natriuretic peptide (ANP), aldosterone and free aldosterone were investigated in ten women between weeks 29 and 33 of normal pregnancy. Hormone levels were studied during unrestricted sodium intake and on day 6 of a low sodium diet. On both occasions venous blood was obtained in the sitting as well as in the left lateral tilt position. Plasma concentrations of ANP during the unrestricted sodium intake were not raised compared with control values in healthy non-pregnant females. Recovery experiments showed no differences in the degradation of ANP in blood from pregnant and non-pregnant women. Plasma concentrations of ANP significantly decreased (by 32%) in response to the low sodium regime in both positions. Concentrations of aldosterone and free aldosterone (in women in the sitting position) increased twofold after sodium restriction. Mean values of ANP were higher in women in the left lateral tilt position that in those in the sitting position, but the difference was not significant. Concentrations of aldosterone and free aldosterone were significantly lower (by around 30%) in women in the left lateral tilt position compared with those in the sitting posture. Journal of Endocrinology (1990) 124, 507–513


1978 ◽  
Vol 45 (6) ◽  
pp. 870-874 ◽  
Author(s):  
F. H. Leenen ◽  
P. Boer ◽  
G. G. Geyskes

Changes in heart rate, blood pressure, and plasma renin activity (PRA) were assessed during infusion of increasing doses of isoproterenol and during increasing work loads of dynamic exercise in five normal young men. Studies were performed at three levels of dietary sodium restriction: normal, moderately, and more severely restricted. Isoproterenol induced the expected dose-related increases in heart rate, systolic blood pressure, and PRA and decreases in diastolic blood pressure. Changes in dietary sodium intake affected these changes only to a minor degree. Dynamic exercise also induced the expected work-load-related increases in heart rate, systolic blood pressure, and PRA and decreases in diastolic blood pressure. Also these changes were not significantly affected by changes in dietary sodium intake. Apparently dietary sodium restriction does not sensitize the renin-releasing mechanisms to sympathetic stimulation.


Sign in / Sign up

Export Citation Format

Share Document