metabolism, it can be presumed that in mild arterial hypertension, defense
mechanisms against intercellular accumulation of zinc are started and it
results in high values of efflux rate constants, significantly higher than in
the group of healthy people, despite lowered Zn-s (reduced electrochemical
gradient). In the process of hypertension development, there is a slowing
down of zinc efflux and its accumulation in cells of heart, wall of
vessels, skeletal muscles, and liver (16,17), which might provide functional
and structural organ changes, characteristic of arterial hypertension.
In the provided research, in the entire tested population, the negative
correlation between ERCt-Zn and age was proved. It is consistent with the
view that with age there are increases in the intercellular content of zinc
and the activity of transcytomembrane ion exchange decreases (11).
The statistically significant negative correlations of ERC of Zn with
values of sRR and dRR in the group of healthy people and in the entire
group of 136 tested people were observed. Together with the increase of
arterial hypertension, Zn-l decreases. In general, the decrease of ERC of
zinc from lymphocytes together with the increase of arterial hypertension
and analyzing interactions of Zn-l and ErCt-Zn and ERCos-Zn in the particular
groups of arterial hypertension, the decrease of Zn-l already in the
MIAH group in comparison with the control group was proved. At the
same time in this group, the ERC did not decrease; on the contrary, they
significantly increased (Fig. 3). It might be claimed that in the initial period
of the arterial hypertension, the activeness of the outflow of zinc from lymphocytes
is increasing; that is, the redistribution of this element is starting.
The volume of free zinc is redistributed in intracellular space. The increase
of activity of the zinc pump (eliminating zinc from the cell against the electrochemical
gradient) directly attests to the increase of inflow of zinc into
the cell; that is, the increase of activity of outflow must be treated as the
action preventing intercellular accumulation of zinc. In the SAH group, it
finally comes to the decrease of activity of outflow of zinc from the lymphocytes
and setting the new balance level conditioned by the changed
metabolic process in hypertension. It cannot be excluded that the base of
changes mentioned above is determined by a genetically conditioned disorder
of cellular membranes functions.
The results of my own research show that the blockade of the aldosterone
receptor by spironolactone causes the activity increase of the outflow
of zinc ions and also the increase of Zn-l in patients with arterial
hypertension. The activity of zinc outflow correlated positively with the
level of this element in the cell (22).
In the recent research, a positive correlation between Zn-s and ERCt-
Zn was proved. The outflow of zinc from the cell takes place against the
concentration gradient and electrochemical gradient (25), considering that
for maintaining the correct intercellular concentration of zinc together
with the increase of Zn-s, the increase of ERCt-Zn should occur. Taking
into consideration all of the directions of change and the fact that Zn can
be a factor that increases arterial blood pressure, the changes in Zn distri-