In the body of patients with diabetes, the sodium content increases by an average of 10%, which is accompanied by an increase in extravascular (interstitial and / or intracellular) fluid volume. At the same time, the volume of plasma and blood in normal blood pressure remains within the normal range, and even decreases in AH.
P. Weidmann and P. Ferrari (1991) provided convincing evidence that the excess sodium in the body of a diabetic patient is available even before the onset of late complications, which distinguishes diabetes patients from patients with essential (primary) hypertension. According to Feldt- Rasmussen et al. (1987), the main role in the development of hypertension in patients with DM type 1 is played by sodium retention in the body, while the levels of aldosterone, angiotensin II and catecholamines in the blood plasma are reduced. These changes are observed at the earliest stages of involvement of the kidneys in the pathological process, when the excretion of albumin has not yet changed. The peculiarity of patients with diabetes with hypertension is that they have an increased sensitivity of blood pressure to sodium retention, whereas in patients with diabetes with normal blood pressure, this is absent.This explains the pronounced hypotensive effect from the use of various measures aimed at increasing sodium excretion (diuretics, dialysis) in patients with diabetes.
Along with this, a definite condition for the more frequent development of hypertension in diabetes is an increase in sensitivity to norepinephrine and angiotensin. The findings suggest that in patients with diabetes the same pressure effect, as in practically healthy individuals, causes noradrenaline and angiotensin II in lower doses. Hyperinsulinemia and insulin resistance have also been found to contribute to an increase in blood pressure, causing an increase in sodium and water retention in the body through direct effects on the distal renal tubules and, indirectly, by increasing the activity of the sympathetic nervous system. It is believed that an additional component of the action of insulin, which leads to sodium retention in the body,is the ability of insulin to increase club filtration of glucose and at the same time enhance the activity of the sodium-glucose transporter (importer), which, like other glucose transporters, is activated when the insulin is integrated with the receptor in the respective target tissues. In addition, insulin regulates the reabsorption of sodium in the tubules indirectly, through the mechanisms of its effect on potassium or by reducing the tubular response to the atrial natriuretic peptide.
In studies conducted in recent years, it has been shown that patients who are resistant to the metabolic action of insulin remain sensitive to the sodium-retaining effect of insulin, which leads to an increase in total sodium and water in the body due to its effect on blood pressure. In addition, insulin promotes sodium retention through stimulation of Na + / K + -ATPases, which mediate sodium transport across the cell membrane.
In recent years, additional data have been obtained indicating that the susceptibility to hypertension and its development in diabetes is based on a violation of the sodium-lithium countercurrent (Na / Li is a cation-exchange pump) and sodium-hydrogen anti-port ( Na / H is a cationic exchanger), the dysfunction of which is observed in nephropathy and, probably, mediates its development. The sodium-hydrogen anti-port in the body performs important functions for maintaining intracellular ion balance by continuously exchanging cations (extracellular sodium ions for intracellular hydrogen in a 1: 1 ratio) through the cell membrane, adjusting the intracellular pH. In addition, the cationic exchanger is involved in controlling the cell volume, its differentiation and proliferation.An increase in the functional state of the cationic exchanger is observed in patients with type 1 diabetes with or without nephropathy, which, according to LL Li et al. (1994) indicates a predisposition to the development of essential hypertension, rather than nephropathy.