The imbalance between consumption of salt and its elimination leads to a change in the filling of the vascular system (fluid volume), which changes the blood pressure level, i.е. in real time, the pressure level determines the ability of the kidneys to remove sodium – this relationship was called the "pressure – natriuresis curve". This ratio is continuously changing, converging to equilibrium. It is important to remember that healthy kidneys can withstand the load of salt, about 40–50 times higher than the normal level of the Na+ daily requirement. The current level of knowledge allows us to consider that the mechanisms ensuring the retention of Na+ (ion exchange pumps), in case of excessive salt intake do not have time to reabsorb the proper amount of Na+ cations at the level of the proximal tubules and the ascending limb of the Henle loop. The largest recent studies have shown that a significant amount of sodium can accumulate in the interstitium without causing fluctuations in the plasma sodium concentration and a compensatory increase in the retention of H2O, i.e. with a constant blood sodium concentration, the total sodium level can vary significantly. Glycosaminoglycans (GAGs) "soften" the fluctuations in the plasma sodium concentration, "hide" sodium from the osmoreceptors, which prevents process of increasing vasopressin secretion and the growth of water retention, mandatory in such a situation. On the other hand, the deposited sodium cations do not reach the nephron, which makes them difficult to excrete from the body. With a decrease in the level of sodium intake, the GAGs polymerization decreases, the decrease in GAGs is accompanied by a massive release of sodium from the reserve. With prolonged overload of GAGs by sodium, damage to macromolecules occurs, and the buffer properties of GAGs are violated. In particular, in salt-sensitive patients this will lead to a sharp increase in blood pressure, patients with in CHF – to the RAAS hyperactivation. We can assume a certain parallelism between sodium intake and GAG level in the interstitial tissue, which is necessary for its accumulation. The change in the ratio of the structural components of tissues will lead to a change in their properties, incl. physical, for example, myocardium stiffness, its elastic properties, arterial stiffness, and striated muscle exercise capacity.

Keywords: sodium, natriuresis, glycosaminoglycans, sodium deposition