Tristan Loscha
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- Dec 18, 2018
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High-Salt Augments Aldosterone Toxicity Despite Lowered Plasma-Readings.
Blood-LVL-Aldosterone gets lowered by sodium,but apparently sensitivity rises,augmenting
damage.Sodium is truly almost a micronutrient,with intakes as low as 500mg-1500mg,in indigenous tribes,lower than
magnesium,lower than calcium,severely lower than potassium.
Thoughts?
Effect of aldosterone and mineralocorticoid receptor blockade on vascular inflammation
Hylton V Joffe, Gail K Adler
Heart failure reviews 10 (1), 31-37, 2005
Aldosterone, the final product of the renin-angiotensin-aldosterone system, is classically viewed as a regulator of renal sodium and potassium handling, blood volume, and blood pressure. Recent studies suggest that aldosterone can cause microvascular damage, vascular inflammation, oxidative stress and endothelial dysfunction. In animal models, aldosterone-mediated vascular injury in the brain, heart, and kidneys leads to stroke, myocardial injury, and proteinuria. These effects may be modified by dietary salt intake; aldosterone-mediated vascular damage is increased in susceptible animals fed a high-salt diet compared to a low-salt diet despite lower plasma aldosterone levels on the high-salt diet. In humans, there is a growing literature supporting the adverse effects of aldosterone in heart failure, hypertension, left ventricular hypertrophy, and renal disease. Aldosterone receptor antagonists are beneficial even in patients on angiotensin converting enzyme inhibitors and attenuate aldosterone-mediated vascular injury by mechanisms that appear to be independent of changes in systolic blood pressure. This review focuses on the adverse effects of aldosterone on the vascular system and describes our current understanding of the underlying mechanisms for this injury.
Furthermore,
Sodium-related:
Dietary salt intake is related to inflammation and albuminuria in primary hypertensive patients
R Yilmaz, H Akoglu, B Altun, T Yildirim, M Arici, Y Erdem
European Journal of Clinical Nutrition 66 (11), 1214, 2012
RESULTS:
Systolic and diastolic BP measurements of patients were similar in the three salt-intake groups. CRP and urinary albumin levels were significantly higher in high-salt-intake group compared with medium-and low-salt-intake groups (P= 0.0003 and P= 0.001, respectively). CRP was positively correlated with 24-h urinary sodium excretion (r= 0.28, P= 0.0008) and albuminuria, whereas albuminuria was positively correlated with 24-h urinary sodium excretion (r= 0.21, P= 0.0002). Multiple regression analysis revealed that urinary sodium excretion was an independent predictor of both CRP and albuminuria.
CONCLUSIONS:
These findings suggest that high salt intake is associated with enhanced inflammation and target organ damage reflected by increased albuminuria in treated hypertensive patients independent of any BP effect.
Blood-LVL-Aldosterone gets lowered by sodium,but apparently sensitivity rises,augmenting
damage.Sodium is truly almost a micronutrient,with intakes as low as 500mg-1500mg,in indigenous tribes,lower than
magnesium,lower than calcium,severely lower than potassium.
Thoughts?
Effect of aldosterone and mineralocorticoid receptor blockade on vascular inflammation
Hylton V Joffe, Gail K Adler
Heart failure reviews 10 (1), 31-37, 2005
Aldosterone, the final product of the renin-angiotensin-aldosterone system, is classically viewed as a regulator of renal sodium and potassium handling, blood volume, and blood pressure. Recent studies suggest that aldosterone can cause microvascular damage, vascular inflammation, oxidative stress and endothelial dysfunction. In animal models, aldosterone-mediated vascular injury in the brain, heart, and kidneys leads to stroke, myocardial injury, and proteinuria. These effects may be modified by dietary salt intake; aldosterone-mediated vascular damage is increased in susceptible animals fed a high-salt diet compared to a low-salt diet despite lower plasma aldosterone levels on the high-salt diet. In humans, there is a growing literature supporting the adverse effects of aldosterone in heart failure, hypertension, left ventricular hypertrophy, and renal disease. Aldosterone receptor antagonists are beneficial even in patients on angiotensin converting enzyme inhibitors and attenuate aldosterone-mediated vascular injury by mechanisms that appear to be independent of changes in systolic blood pressure. This review focuses on the adverse effects of aldosterone on the vascular system and describes our current understanding of the underlying mechanisms for this injury.
Furthermore,
Sodium-related:
Dietary salt intake is related to inflammation and albuminuria in primary hypertensive patients
R Yilmaz, H Akoglu, B Altun, T Yildirim, M Arici, Y Erdem
European Journal of Clinical Nutrition 66 (11), 1214, 2012
RESULTS:
Systolic and diastolic BP measurements of patients were similar in the three salt-intake groups. CRP and urinary albumin levels were significantly higher in high-salt-intake group compared with medium-and low-salt-intake groups (P= 0.0003 and P= 0.001, respectively). CRP was positively correlated with 24-h urinary sodium excretion (r= 0.28, P= 0.0008) and albuminuria, whereas albuminuria was positively correlated with 24-h urinary sodium excretion (r= 0.21, P= 0.0002). Multiple regression analysis revealed that urinary sodium excretion was an independent predictor of both CRP and albuminuria.
CONCLUSIONS:
These findings suggest that high salt intake is associated with enhanced inflammation and target organ damage reflected by increased albuminuria in treated hypertensive patients independent of any BP effect.
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