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Sodium and potassium fluxes and concentrations in erythrocytes of normal subjects during prolonged sodium depletion and repletion.

TLDR
The long-term effect of dietary sodium restriction and repletion suggests either the involvement of a mechanism which can only be slowly reversible or a mechanisms which is irreversible so that normalization takes place only when new red cells are released into the circulation.
Abstract
The erythrocyte concentration and fluxes of sodium and potassium were investigated in normal white male subjects during dietary sodium restriction and repletion, each period lasting for 16 weeks. During dietary sodium restriction the intra-erythrocyte sodium concentration decreased and the red cell ouabain-sensitive 86Rb-uptake increased; no significant changes were observed in the ouabain-insensitive fluxes of sodium such as the total, frusemide-resistant and frusemide-sensitive Na+-efflux and the Na+, Li+-countertransport. The decrease in the intra-erythrocyte sodium concentration could result from an increased Na+,K+-ATPase pump activity. The latter increase could be secondary to the early decrease in a digitalis-like plasma inhibitor and the late increase could be facilitated by the late rise in the intracellular ATP concentration, which is the energy supplier for this pump. During the subsequent first month of sodium repletion the intra-erythrocyte sodium concentration remained low, the red cell ouabain-sensitive 86Rb-uptake and ATP concentration remained elevated and returned to baseline only after 16 weeks. This long-term effect suggests either the involvement of a mechanism which can only be slowly reversible or a mechanism which is irreversible so that normalization takes place only when new red cells are released into the circulation.

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By how much does dietary salt reduction lower blood pressure? III--Analysis of data from trials of salt reduction.

TL;DR: The results from the trials support the estimates from the observational data, and the effect of universal moderate dietary salt reduction on mortality from stroke and ischaemic heart disease would be substantial--larger than could be achieved by fully implementing recommended policy for treating high blood pressure with drugs.
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TL;DR: Responses of blood pressure to alterations in the intake of sodium chloride vary widely between individuals, which complicates investigations of mechanisms responsible for salt sensitivity and limits the appeal of salt restriction as a nonpharmacological antihypertensive therapy.
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Iptakalim protects PC12 cell against H2O2-induced oxidative injury via opening mitochondrial ATP-sensitive potassium channel.

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Alterations in sodium metabolism as an etiological model for hypertension.

TL;DR: This review article describes how this abnormal sodium and calcium metabolism translates into increased systemic vascular resistance through altered vasoactive responses and/or vasculature structural changes.
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Erythrocyte concentrations and transmembrane fluxes of sodium and potassium in essential hypertension: role of intrinsic and environmental factors.

TL;DR: It is suggested that an adequate matching for race, sex, stage of the menstrual cycle (in women), family history of hypertension, and the amount of sodium in the diet should be a prerequisite for valid conclusions when interpreting the erythrocyte concentration and fluxes of sodium.
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