Zinc Balance Normalization
An Important Mechanism
of Angiotensin-Converting Enzyme Inhibitors
and Other Drugs Decreasing the Activity
of the Rennin–Angiotensin–Aldosterone System
Faculty of Physical Education and Physiotherapy, Institute
of Technology, Opole, and Clinic of Cardiology, Medical
aw, Prószkowska Street 76, 45-758 Opole, Poland
Received May 22, 2006; Accepted June 10, 2006
Imbalances of zinc (Zn) metabolism in arterial hypertension are
related to increased urinary Zn excretion, Zn transfer between extracellu-
lar and intracellular spaces, and redistribution of this element inside the
cells. The changes include an increase of the absorption of Zn in the gas-
trointestinal tract and decreases of its concentration in lymphocytes, bone,
and arterial walls. The Zn content of erythrocytes, cardiac muscle, and kid-
neys also increases. The condition eventually leads to Zn deficiency (1–5).
Zinc plays many roles in biological systems. It is a component of over
300 enzymes, performing catalytic, cocatalytic, and/or structural func-
tions. Among others, it conditions the activities of carbonic anhydrase
(CA) and the angiotensin-I converting (ACE) and endothelin-converting
(EC) enzymes. Zn is essential for forming the quaternary structure of
numerous regulatory proteins and hormone receptors that conditions
binding with DNA, such as zinc-fingers, zinc-twists, or zinc-clusters. It is
a structural element of the nucleic acids and takes part in its metabolism.
Zn stabilizes and regulates cell membrane functions. Cellular growth and
division depends on the content of Zn inside the cell and on its transport
inside the cell’s compartments (6–11).
Zinc is able to mobilize calcium from its location within the cell, and
in this way, it modifies calcium-dependent processes inside the cell. It
exerts an inhibitory effect on the ATP-dependent pump that causes the
efflux of Ca
ions from cells to extracellular compartments.
Biological Trace Element Research
Vol. 115, 2007
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