bution can be regarded as having, to a certain extent, a protective character
leading to weakeninig of the pressor reaction, assuming a genetic existence
of relative or absolute Zn excess in the body. The changes of Zn
distribution can lead, after some time, to Zn deficiency and metabolic
changes resulting from it (i.e., carbohydrate intolerance).
Similar directions of changes in metabolism of zinc in diabetes mellitus
(26) and obesity (27) might explain the higher dynamics of organ
changes in the occurrence of the coexistence of arterial hypertension, diabetes,
and obesity.
CONCLUSIONS
1. In primary arterial hypertension, the decrease of zinc concentration
in serum and the decrease of zinc content in lymphocytes
was confirmed.
2. Outflow constants of zinc from lymphocytes in patients with
mild arterial hypertension are higher than in the group of
healthy people.
3. Outflow constants of zinc from the lymphocytes at patients
with moderate arterial hypertension do not differing significantly
in comparison to the group of healthy people.
4. Outflow constants of zinc from the lymphocytes at patients
with severe arterial hypertension are lower than in the group
of healthy people.